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Cystic kidney disease in tuberous sclerosis complex: current knowledge and unresolved questions
|
Regarding cystic kidney disease in pediatric TSC, which of the following is true? a) Large symptomatic cysts have the highest risk of undergoing malignant transformation. b) Mutations in TSC1 confer a higher risk of kidney failure due to severe polycystic disease and requiring more aggressive therapeutic interventions. c) The Bosniak classification is helpful to stratify cystic kidney masses according to their malignant potential and determine the need and timing of follow-up imaging. d) Temporal changes in cyst morphology are the best indicators of their malignant potential.
|
d
|
Cystic kidney disease in tuberous sclerosis complex: current knowledge and unresolved questions
|
Which of the following statements about mTOR inhibitors (mTORi) is false? a) Tacrolimus, sirolimus, and everolimus all inhibit mTOR activity. b) mTORi is often used to treat the kidney manifestations of TSC. c) It is unclear if TSC-associated kidney cysts respond to mTORi treatment. d) Pharmacologic levels of mTORi only partly replace the normal function of the TSC1 and TSC2 proteins.
|
a
|
Cystic kidney disease in tuberous sclerosis complex: current knowledge and unresolved questions
|
In a 7-year-old boy with a clinical diagnosis of TSC based on brain and skin findings, which of the following is most consistent with a diagnosis of TSC/PKD contiguous gene syndrome? a) Bilateral kidney cysts, hypertension, and a disease-associated point mutation in exon 8 of the TSC2 gene b) Bilateral kidney cysts, hypertension, and a paternal grandfather on dialysis for ADPKD c) Bilateral kidney cysts, hypertension, and deletion of multiple exons at the 3’ end of the TSC2 gene d) Bilateral kidney cysts, hypertension, and deletion of multiple exons at the 3’ end of the TSC1 gene
|
c
|
Diabetic kidney disease in children and adolescents: an update
|
1. Which of the following statements is correct about diabetic kidney disease? a) It is always associated with proteinuria. b) It never progresses to end-stage renal disease. c) It can be slowed with appropriate glycemic control. d) It is reversible with medication.c2. What is a common early marker of diabetic kidney disease? a) Microalbuminuria b) Hyperglycemia c) Hypoglycemia d) Polyuriaa3. Which medication is commonly used to treat diabetic kidney disease? a) ACE inhibitors b) Beta-blockers c) Calcium channel blockers d) Diureticsa4. What lifestyle modification is recommended to prevent diabetic kidney disease progression? a) Increased protein intake b) Decreased physical activity c) Smoking cessation d) Increased sodium intakec5. Which of the following is a risk factor for developing diabetic kidney disease in children? a) Low blood pressure b) Type 1 diabetes c) Non-diabetic parents d) Normal weightb
|
c
|
Diabetic kidney disease in children and adolescents: an update
|
2. What is a common early marker of diabetic kidney disease? a) Microalbuminuria b) Hyperglycemia c) Hypoglycemia d) Polyuria
|
a
|
Diabetic kidney disease in children and adolescents: an update
|
3. Which medication is commonly used to treat diabetic kidney disease? a) ACE inhibitors b) Beta-blockers c) Calcium channel blockers d) Diuretics
|
a
|
Diabetic kidney disease in children and adolescents: an update
|
4. What lifestyle modification is recommended to prevent diabetic kidney disease progression? a) Increased protein intake b) Decreased physical activity c) Smoking cessation d) Increased sodium intake
|
c
|
Diabetic kidney disease in children and adolescents: an update
|
5. Which of the following is a risk factor for developing diabetic kidney disease in children? a) Low blood pressure b) Type 1 diabetes c) Non-diabetic parents d) Normal weight
|
b
|
Early microvascular complications in type 1 and type 2 diabetes
|
You are seeing a 14-year-old female patient who has had type 1 diabetes for a total of 5 years in diabetes clinic. Your patient and her family are interested in learning more about the complications of diabetes. Which of the following do you advise the family is the most common microvascular complication of diabetes?\na. Diabetic kidney disease\nb. Diabetic eye disease\nc. Diabetic nerve disease\nd. Cardiovascular disease
|
b
|
Early microvascular complications in type 1 and type 2 diabetes
|
Which of the following most accurately describes the onset and progression of diabetic kidney disease in children with type 2 diabetes compared to children with type 1 diabetes?\na. Diabetic kidney disease is more prevalent at onset in type 2 diabetes, but available evidence suggests it progresses at a slower rate.\nb. Diabetic kidney disease is more prevalent at onset in type 2 diabetes, and available evidence suggests it progresses at a faster rate.\nc. Although early diabetic kidney disease may exist at diagnosis in type 2 diabetes, the long-term risk of chronic kidney disease progression is similar to type 1 diabetes.\nd. It is extremely rare for early diabetic kidney disease to be present at diagnosis in either type 1 or type 2 diabetes, and the risk of long-term progression of chronic kidney disease is similar for both conditions.
|
b
|
Early microvascular complications in type 1 and type 2 diabetes
|
You are caring for an 18-year-old male patient with type 2 diabetes who has recently developed worsening albuminuria, which has now progressed to macroalbuminuria. He is currently receiving treatment with metformin and lisinopril. His HbA1c is above target at 7.5% and he has a normal serum creatinine. Which of the following is the best option to improve his long-term kidney outcome?\na. Initiation of long-acting insulin\nb. Addition of an angiotensin-receptor blocker (ARB)\nc. Initiation of a glucagon-like peptide 1 receptor agonist (GLP-1 RA)\nd. Initiation of a sodium-glucose co-transporter 2 (SGLT2) inhibitor
|
d
|
Early microvascular complications in type 1 and type 2 diabetes
|
Which of the following most accurately describes the patient that is at highest risk for developing retinopathy?\na. A 16-year-old male patient with type 1 diabetes diagnosed at 15 years of age with an HbA1c of 7.5% and no microalbuminuria.\nb. An 8-year-old male patient with type 1 diabetes diagnosed at 2 years of age with an HbA1c of 8% and no microalbuminuria.\nc. A 16-year-old female patient with type 1 diabetes diagnosed at age 7 years with an HbA1c of 11% and microalbuminuria.\nd. An 18-year-old female patient with type 1 diabetes diagnosed at age 15 years with an HbA1c of 9% and microalbuminuria.
|
c
|
Early microvascular complications in type 1 and type 2 diabetes
|
You are evaluating a 16-year-old male with a 4-year history of very poorly controlled type 2 diabetes (HbA1c > 14% now) on combination therapy with metformin and long-acting insulin who presents with numbness and tingling in his bilateral lower extremities. What is your next step for further evaluation and/or treatment of this finding?\na. Order cardiovascular reflex testing including heart rate variability and an EKG to evaluate the QT interval.\nb. Start treatment with gabapentin.\nc. Recommend improved glycemic control and increase the patient’s long-acting insulin by 20%.\nd. Start treatment with a glucagon-like peptide 1 receptor agonist (GLP-1 RA).
|
a
|
Endothelial dysfunction as a factor leading to arterial hypertension
|
Indicate incorrect answer for nitric oxide (NO): a) NO is the main endothelium-derived vasodilatator b) Potassium has an opposite function to NO c) The main substrate to produce NO is arginine d) NO inhibits platelet aggregation and adhesion, smooth muscle cell proliferation, and leucocyte adhesion e) NO inhibits vascular permeability and inflammatory mechanisms
|
b
|
Endothelial dysfunction as a factor leading to arterial hypertension
|
Which antihypertensive drug has no beneficial effect on endothelial cells: a) Valsartan b) Amlodipine c) Ramipril d) Metoprolol e) Nebivolol
|
d
|
Endothelial dysfunction as a factor leading to arterial hypertension
|
What is the biomarker of glycocalyx damage? a) Syndecan-1 b) Angiopoietin-2 c) Angiotensin II d) A + B e) A + C
|
d
|
Endothelial dysfunction as a factor leading to arterial hypertension
|
Which of the following statements about glycocalyx (GCX) is true: a) It has only a mechanical function b) Injury to the GCX increases the risk of atherosclerosis c) Decreased heparanase activity leads to GCX damage d) Loss of GCX decreases transcapillary albumin transport e) GCX damage does not affect vascular permeability
|
b
|
Endothelial dysfunction as a factor leading to arterial hypertension
|
Which of the following methods is not used to evaluate endothelial function in children in studies? a) FMD b) Albuminuria c) Endocan level d) Thrombomodulin level e) Quantitative coronary angiography
|
e
|
Fabry disease and kidney involvement
|
What are the clinical manifestations in patients with FD? a) only gastrointestinal symptoms and neuropathic pain b) symptoms and signs are heterogeneous c) kidney failure d) heart failure e) gastrointestinal symptoms, neuropathic pain, angiokeratoma, hypohidrosis, acroparesthesia and discomfort during adulthood
|
b
|
Fabry disease and kidney involvement
|
When does Gb-3 deposition occur in the kidney? a) as early as during fetal development b) only after the age of 10 c) in adulthood d) during fetal development only in female patients e) in old age
|
a
|
Fabry disease and kidney involvement
|
Kidney involvement is: a) a positive prognostic indicator b) an early sign of Fabry disease c) a sure predictor of therapy failure d) a significant cause of morbidity and reduced life expectancy in patients with Fabry’s disease e) present only in the elderly
|
d
|
Fabry disease and kidney involvement
|
What is the main therapy? a) diet and exercise b) enzyme replacement therapy (ERT) with glucocerebrosidase c) dialysis d) enzyme replacement therapy (ERT) with agalsidase alfa and agalsidase beta e) lifestyle change
|
d
|
Fabry disease and kidney involvement
|
What are the initial manifestations of kidney impairment? a) shortness of breath b) decreased urine output c) fatigue and confusion d) an increase in microalbuminuria and proteinuria e) a decrease in creatinine clearance
|
d
|
Erythropoiesis-independent effects of iron in chronic kidney disease
|
In children with CKD, serum ferritin INVERSELY correlates with:\na) CKD stage\nb) Serum hepcidin\nc) Hemoglobin\nd) Inflammatory markers\ne) Iron sequestration
|
c
|
Erythropoiesis-independent effects of iron in chronic kidney disease
|
Hepcidin regulates cellular iron transport by binding to:\na) Ferritin heavy chain\nb) Ferritin light chain\nc) Transferrin receptor 1\nd) Ferroportin\ne) Erythroferron
|
d
|
Erythropoiesis-independent effects of iron in chronic kidney disease
|
Ferroportin is…:\na) …iron importer highly expressed on the apical aspect of enterocytes.\nb) …not expressed in tubular epithelial cells.\nc) …a transcription factor regulating intracellular iron balance.\nd) …regulated exclusively by systemic hepcidin in all cell types.\ne) …the only known iron exporter.
|
e
|
Erythropoiesis-independent effects of iron in chronic kidney disease
|
Which of the following statements about physiologic renal iron handling is correct?\na) Iron is not filtered by healthy glomeruli but may be filtered in nephrotic syndrome.\nb) Iron is filtered by the glomeruli and the majority of filtered iron is reabsorbed.\nc) Tubular secretion of iron is critically important for maintaining iron balance.\nd) Iron is reabsorbed in the proximal tubule primarily via brush border ferroportin.\ne) Transferrin-bound iron cannot be reabsorbed because tubular epithelial cells do not express transferrin receptor 1.
|
b
|
Erythropoiesis-independent effects of iron in chronic kidney disease
|
Choose the correct statement about the relationship between iron, mineral homeostasis, and bone health:\na) In clinical trials, ferric citrate coordination complex improved hyperphosphatemia in adult dialysis patients.\nb) All iron preparations stimulate FGF23 production in patients with CKD.\nc) Hypophosphatemia has been reported as a complication of oral, but not parenteral, iron administration.\nd) In the general population, similar to children with thalassemia, total body iron stores are directly associated with improved bone mineral density.\ne) Iron typically stimulates the function of osteoblasts and inhibits the function of osteoclasts.
|
a
|
Genetic causes of neonatal and infantile hypercalcaemia
|
Neonatal severe hyperparathyroidism (NSHPT) and familial hypocalciuric hypercalcaemia (FHH) are: a) Both caused by inactivating mutations in the CaSR gene only. b) NSHPT is caused by inactivating mutations in the CaSR only; FHH is caused by inactivating mutations in the CaSR, Gα11 and AP2σ genes. c) NSHPT is caused by inactivating mutations in the CaSR, Gα11 and AP2σ genes; FHH is caused by inactivating mutations in the CaSR gene only. d) Both are caused by inactivating mutations in the CaSR, Gα11 and AP2σ genes.
|
b
|
Genetic causes of neonatal and infantile hypercalcaemia
|
Jansen’s metaphyseal chondrodysplasia is characterised by: a) Short-limbed short stature, deformed, under-mineralised bones, chronic hypercalcaemia and hypophosphaturia with elevated serum PTH levels and elevated serum markers of bone turnover. b) Short-limbed short stature, deformed, under-mineralised bones, chronic hypercalcaemia and hypophosphaturia with normal serum PTH levels and elevated serum markers of bone turnover. c) Short-limbed short stature, deformed, under-mineralised bones, transient hypercalcaemia and hyperphosphaturia with normal serum PTH levels and elevated serum markers of bone turnover. d) Short-limbed short stature, deformed, under-mineralised bones, chronic hypercalcaemia and hypophosphaturia with normal serum PTH levels and elevated serum markers of bone turnover.
|
d
|
Genetic causes of neonatal and infantile hypercalcaemia
|
Idiopathic infantile hypercalcaemia (IIH) is caused by mutations in: a) The CYP27B1 gene, encoding 1α-hydroxylase, which converts 25-hydroxyvitamin D3 to active 1,25(OH)2D3. b) The CYP24A1 gene, encoding 24-hydroxylase, which inactivates 1,25(OH)2D3. c) The CYP2R1 gene, encoding 25-hydroxylase, which converts vitamin D to 25-hydroxyvitamin D3. d) The CYP24A1 and CYP27B1 genes. e) The CYP2R1, CYP24A1 and CYP27B1 genes.
|
b
|
Genetic causes of neonatal and infantile hypercalcaemia
|
In Williams syndrome the reported frequency of hypercalcaemia is: a) >50%, is often symptomatic, may resolve within the first few years, but may recur during puberty. b) <50%, is often symptomatic, may resolve within the first few years, but may recur during puberty. c) <50%, is often asymptomatic, and always resolves within the first few years, with no recurrence. d) >50%, is often asymptomatic, and always resolves within the first few years, with no recurrence.
|
b
|
Genetic causes of neonatal and infantile hypercalcaemia
|
Which of these causes of hypercalcaemia is characterised by poor feeding, rachitic deformities that can result in respiratory complications, persistent rickets, bony craniosynostosis and is associated with mutations in the ALPL gene: a) Jansen’s metaphyseal chondrodysplasia b) William’s syndrome c) Hypophosphatasia d) Blue diaper syndrome e) Subcutaneous fat necrosis of the newborn
|
c
|
Gutted constipation in children with chronic kidney disease and on dialysis
|
Factors contributing to constipation in children with CKD include:<br>a) Reduced fluid intake as kidney function deteriorates<br>b) Toileting behaviors<br>c) Reduction in physical activity<br>d) Medications used in the management of CKD<br>e) All of the above
|
e
|
Gutted constipation in children with chronic kidney disease and on dialysis
|
The understanding of gut dysbiosis is important in CKD because:<br>a) There is evidence that it directly leads to disease progression<br>b) Evidence suggests some increased cardiovascular risk<br>c) Dysregulation leads to worsening uremia<br>d) b and c<br>e) All of the above
|
e
|
Gutted constipation in children with chronic kidney disease and on dialysis
|
Children on dialysis who are constipated, can have hyperkalemia. This can be due to:<br>a) CKD leads to an intracellular accumulation of potassium<br>b) Constipation reduces intestinal transit time, leading to increased potassium absorption<br>c) In healthy individuals up to 80% of potassium is excreted through the gastrointestinal tract<br>d) All laxatives contain potassium salts<br>e) All of the above
|
b
|
Gutted constipation in children with chronic kidney disease and on dialysis
|
Which of these laxatives has the highest sodium content?<br>a) Isotonic Polyethylene Glycol (PEG)<br>b) Ispaghula husk<br>c) Docusate sodium<br>d) Bisacodyl<br>e) Sodium picosulphate
|
a
|
Gutted constipation in children with chronic kidney disease and on dialysis
|
Children with CKD requiring pharmacological management of constipation:<br>a) Are more often on peritoneal dialysis than hemodialysis<br>b) Often require one agent for optimal management<br>c) Require care to be taken when prescribing multiple agents as they may contain sodium and potassium salts<br>d) Require large volumes of laxatives for optimal management<br>e) Require large volumes of fluid for optimal management
|
c
|
How to define and assess the clinically significant causes of hematuria in childhood
|
What is the most common cause of macroscopic post-glomerular hematuria in childhood? a) IgA nephropathy b) Nutcracker syndrome, arteriovenous malformations c) Nephrolithiasis, hypercalciuria d) Bladder tumor
|
c
|
How to define and assess the clinically significant causes of hematuria in childhood
|
What is the prognosis of IgA nephropathy in childhood? a) It usually leads to rapidly progressive glomerulonephritis b) It is commonly a benign condition, but a considerable percentage of patients will develop chronic kidney disease c) Is always a benign self-limiting condition d) Its prognosis depends on the number of acquired infections in childhood
|
b
|
How to define and assess the clinically significant causes of hematuria in childhood
|
When would you indicate a kidney biopsy in childhood in the process of evaluating hematuria? a) Hematuria cases with persisting acute kidney injury or chronic kidney injury with unknown origin b) In every case of nephrotic syndrome c) To verify Alport syndrome with a positive family background d) In every case of persisting microscopic hematuria
|
a
|
How to define and assess the clinically significant causes of hematuria in childhood
|
What is the cornerstone of radiological imaging in suspected childhood nephrolithiasis? a) Magnetic resonance imaging b) Low-dose computed tomography c) Ultrasound with the combination of cystoscopy d) Ultrasound
|
d
|
How to define and assess the clinically significant causes of hematuria in childhood
|
Which of the following statements is true for hematuria in childhood? a) Hematuria is a common finding in idiopathic nephrotic syndrome in childhood. b) Macroscopic hematuria found in Henoch-Schönlein purpura always has an origin of bladder hemorrhage. c) The combination of hematuria and proteinuria can be a sign of progressive kidney disease. d) Hematuria during urinary tract infection is a hallmark of glomerular damage.
|
c
|
How to take advantage of easily available biomarkers in patients with IgA nephropathy: IgA and C3 in serum and kidney biopsies
|
1. IgA nephropathy: a. is the most common nephropathy in the world b. can lead to kidney failure in 20–40% of patients within 20 years c. is most prevalent in Asians, followed by Caucasians, and relatively rare in Africans d. kidney biopsy is the gold standard diagnostic method e. the diagnosis is made based on elevated serum IgA level
|
a, b, c, d
|
How to take advantage of easily available biomarkers in patients with IgA nephropathy: IgA and C3 in serum and kidney biopsies
|
2. Clinical manifestations of IgA nephropathy include: a. erythrocyturia or hematuria b. proteinuria c. asymptomatic leukocyturia d. hypertension e. kidney failure
|
a, b, d, e
|
How to take advantage of easily available biomarkers in patients with IgA nephropathy: IgA and C3 in serum and kidney biopsies
|
3. Factors important in the pathogenesis of IgA nephropathy include: a. formation of oligoglycosylated IgA1 b. formation of anti-glycan antibodies c. genetic predisposition d. complement activation by the classical pathway e. complement activation by the alternative pathway
|
a, b, c, e
|
How to take advantage of easily available biomarkers in patients with IgA nephropathy: IgA and C3 in serum and kidney biopsies
|
4. Serum IgA level: a. may be elevated in about 50% of patients with IgA nephropathy b. has no prognostic significance c. indicates GDIgA1 d. is related to creatinine level e. is associated with lower proteinuria
|
a, b
|
How to take advantage of easily available biomarkers in patients with IgA nephropathy: IgA and C3 in serum and kidney biopsies
|
5. C3 complement component: a. serum C3 level < 90 mg/dL in adults is an adverse prognostic factor b. serum C3 level correlates positively with the severity of C3 deposits in kidney biopsy c. elevated C3 level is present in patients with the protective CFHR1/CFHR3 deletion d. severe C3 deposits in kidney biopsy are associated with better kidney survival e. may be a component of IgA/C3 and have prognostic significance
|
a, c, e
|
Hypogammaglobulinemia in pediatric kidney transplant recipients
|
Which of the following is an accurate statement pertaining to the epidemiology of hypogammaglobulinemia after kidney transplantation? a) Hypogammaglobulinemia is more common in children than adults after Tx b) The prevalence of hypogammaglobulinemia peaks at 12 months after Tx c) MMF is associated with a higher risk of Ig abnormalities compared to Aza d) Ig abnormalities are rare after Tx in the absence of an underlying primary immunodeficiency
|
c
|
Hypogammaglobulinemia in pediatric kidney transplant recipients
|
Which of the following complications have been associated with post-Tx hypogammaglobulinemia? a) Pneumocystis jirovecii infections b) Secondary malignancies c) Bacterial sepsis d) Rotaviral gastroenteritis
|
c
|
Hypogammaglobulinemia in pediatric kidney transplant recipients
|
Of the following immunosuppressive strategies, which has been shown to be useful in patients who develop post-Tx hypo-IgG and experience recurrent infections, while receiving an MMF-based immunosuppressive regimen? a) Substitute MMF with azathioprine b) Add an IL-2 receptor blocker to the regimen c) Replace MMF with methotrexate d) Start a short course of IV thymoglobulin
|
a
|
Hypogammaglobulinemia in pediatric kidney transplant recipients
|
Which of the following statements pertaining to the treatment of hypogammaglobulinemia after Tx is true? a) Data support the use of IVIG replacement for all patients post-Tx with Ig abnormalities b) More frequent IVIG replacement therapy is required in post-Tx patients compared to those with primary immunodeficiencies c) IVIG therapy is contraindicated after kidney Tx d) There are no controlled trials assessing the role and indication for IVIG after kidney Tx
|
d
|
Hypogammaglobulinemia in pediatric kidney transplant recipients
|
Which of the following statements is true about post-Tx bronchiectasis? a) The use of MMF has been linked to the development of bronchiectasis b) Data clearly support a causal link between Ig abnormalities and post-Tx bronchiectasis c) Post-Tx bronchiectasis is an indication for starting IVIG therapy d) The severity of hypogammaglobulinemia is a strong predictor for the development of bronchiectasis
|
a
|
Non-Hodgkin lymphoma after pediatric kidney transplantation
|
Non-Hodgkin lymphoma (NHL) in patients after kidney transplantation: a) Is a unique and very rare malignancy, seen mainly in adults b) Is a common type of PTLD c) Develops only >10 years after transplantation d) Presents incidence comparable with normal age-matched population e) Is diagnosed only in adolescents after transplantation
|
b
|
Non-Hodgkin lymphoma after pediatric kidney transplantation
|
Non-Hodgkin lymphoma (NHL) after kidney transplantation: a) Is EBV-negative in all cases b) Never develops in CMV-negative patients c) Develops only in EBV-seronegative patients before transplantation d) Is EBV-positive in the majority of pediatric patients e) Never develops in patients presenting EBV reactivation
|
d
|
Non-Hodgkin lymphoma after pediatric kidney transplantation
|
Confirmed associations between immunosuppression and risk of developing NHL include: a) Importance of high exposure to steroids, which must be withdrawn after diagnosis b) Use of anti-IL2R-based blocking induction c) Use of rituximab in the treatment of primary nephrotic syndrome in case-history before transplantation d) Use of belatacept in EBV-negative (at transplant) patients e) Use of moderate doses of rabbit thymoglobulin for induction in EBV-positive patients
|
d
|
Non-Hodgkin lymphoma after pediatric kidney transplantation
|
Therapeutic approach in post-transplant NHL includes: a) Immediate radiation of the malignant lesion, regardless of its localization b) Use of rituximab monotherapy in all cases c) Immediate use of interferon together with rituximab d) Reduction of immunosuppression plus rituximab in B cell-positive cases and specific oncologic protocol, adjusted to the defined staging of the disease and morphology of the malignant lesion e) Intensive antiviral treatment (ganciclovir for 6 months) and with IVIG pulses (2 g/kg) in EBV-positive cases, combined with rituximab
|
d
|
Non-Hodgkin lymphoma after pediatric kidney transplantation
|
In patients who survived NHL and lost the kidney graft: a) Re-transplantation is not possible due to unacceptable, high risk of malignancy recurrence b) Re-transplantation must be postponed >10 years after malignancy c) Immunosuppression in re-transplantation must be reduced and never include biological agents d) Re-transplantation is possible after 2–3 years of malignancy-free period and after gaining immunity against EBV (in previously negative patients) e) Re-transplantation must be performed with prophylactic use of rituximab
|
d
|
Overview of the findings and advances in the neurocognitive and psychosocial functioning of mild to moderate pediatric CKD perspectives from the Chronic Kidney Disease in Children (CKiD) cohort study
|
In the CKiD study, a relatively high percentage of children with mild to moderate CKD can manifest mild neurocognitive difficulties in: a) Impulsivity b) Verbal IQ c) Parent ratings of executive functions d) Anxiety
|
c
|
Overview of the findings and advances in the neurocognitive and psychosocial functioning of mild to moderate pediatric CKD perspectives from the Chronic Kidney Disease in Children (CKiD) cohort study
|
From the CKiD study, there are a variety of factors that have been associated with neurocognitive functioning including: a) Low bicarbonate and low blood pressure variability b) High bicarbonate and high blood pressure variability c) Low bicarbonate and high blood pressure d) High bicarbonate and low blood pressure
|
b
|
Overview of the findings and advances in the neurocognitive and psychosocial functioning of mild to moderate pediatric CKD perspectives from the Chronic Kidney Disease in Children (CKiD) cohort study
|
Children with mild to moderate CKD show: a) Rates of depression that are slightly higher than that found in the normal population b) Extremely high rates of depression c) Extremely high rates of behavior problems d) Extremely low rates of depression
|
a
|
Overview of the findings and advances in the neurocognitive and psychosocial functioning of mild to moderate pediatric CKD perspectives from the Chronic Kidney Disease in Children (CKiD) cohort study
|
On quality of life ratings, parents and youth reported: a) Ratings in the physical and emotional domains to be significantly more impaired when compared to similar reports from healthy children. b) Ratings in the physical domain to be significantly more impaired when compared to similar reports from healthy children. c) Ratings in the physical, school, social, and emotional domains to be equivalent to those from healthy children. d) Ratings in the school and social domains to be significantly higher when compared to similar reports from healthy children.
|
a
|
Overview of the findings and advances in the neurocognitive and psychosocial functioning of mild to moderate pediatric CKD perspectives from the Chronic Kidney Disease in Children (CKiD) cohort study
|
From the CKiD study, best practices would dictate: a) The need for annual comprehensive assessments. b) No need for any comprehensive assessments in this population. c) Appreciation for the various factors contributing to neurocognitive and psychosocial outcomes, including increased consideration for brain imaging and genetic testing strategies, and consideration for routine monitoring of neurocognitive and psychosocial functioning. d) A focus on neurocognitive assessments at more frequent intervals than emotional-behavioral assessments.
|
c
|
Nutritional management of the infant with chronic kidney disease stages 2–5 and on dialysis
|
1. Which of the following statements is true? a) The infant’s weight, length and weight-for-length need only be measured when there are concerns about growth. b) The infant’s euvolemic weight, length and head circumference should be measured frequently and plotted on WHO growth charts. c) True gain in body weight in infants on peritoneal dialysis cannot be distinguished from fluid retention. d) An infant’s failure to gain weight is not a signal for nutritional intervention.
|
b
|
Nutritional management of the infant with chronic kidney disease stages 2–5 and on dialysis
|
2. Which of the following statements is true? a) The energy and protein intake for the conservatively managed infant with CKD should approximate that of the healthy infant. b) The energy and protein intake for the conservatively managed infant with CKD should be 150% higher than the requirements of the healthy infant. c) Infants with CKD on peritoneal dialysis require a lower protein intake than infants managed conservatively. d) The energy derived from glucose in the dialysate should not be included in the energy intake for the infant on peritoneal dialysis.
|
a
|
Nutritional management of the infant with chronic kidney disease stages 2–5 and on dialysis
|
3. Which of the following statements is true? a) Infants with CKD should be fed a renal-specific low potassium formula from birth. b) Infants with CKD can have cow’s milk as their main drink from 6 months of age. c) Breast milk or whey-dominant infant formula are the preferred feeds for infants with CKD throughout the first year. d) Casein-dominant infant formulas have a nutritional profile closest to breast milk.
|
c
|
Nutritional management of the infant with chronic kidney disease stages 2–5 and on dialysis
|
4. Which of the following statements is true? a) Infants with CKD should have a healthy balanced diet avoiding sugars, fats and salt. b) Infants with CKD should avoid foods high in calcium, phosphate and potassium. c) Modification of the calcium, phosphate and potassium content of the diet of the infant with CKD can help maintain normal serum ranges. d) The introduction of solid foods should be delayed in the infant with CKD.
|
c
|
Nutritional management of the infant with chronic kidney disease stages 2–5 and on dialysis
|
5. Which of the following statements is true? a) As soon as the infant’s weight starts to falter, start enteral tube feeding. b) As soon as the infant’s weight starts to falter restrict the intake of phosphate and potassium. c) As soon as the infant’s weight starts to falter, start peritoneal dialysis. d) As soon as the infant’s weight starts to falter, start nutritional supplementation of oral feeds and solid foods.
|
d
|
Palliative care for children and young people with stage 5 chronic kidney disease
|
Advance care planning discussions: a) Should result in an agreement regarding resuscitation and limitations of treatment. b) Are often a series of conversations over a period of time and decisions may change. c) Must be led by a palliative care physician. d) Should only involve the CYP in exceptional circumstances.
|
b
|
Palliative care for children and young people with stage 5 chronic kidney disease
|
When involving CYP in decision-making: a) Child/young person’s age is the most important consideration. b) Clinician should meet with the child/young person alone. c) Child/young person’s wishes should take precedence over the wishes of parents. d) Child/young person should determine degree and timing of disclosure of information about care, treatment, condition, and prognosis.
|
d
|
Palliative care for children and young people with stage 5 chronic kidney disease
|
When selecting an opioid for pain management in CKD 5: a) Morphine should be avoided due to accumulation. b) Oxycodone is a good option for a long-acting opioid. c) Fentanyl or alfentanyl are the preferred option for a continuous infusion. d) The opioid dosing interval should generally be reduced.
|
c
|
Palliative care for children and young people with stage 5 chronic kidney disease
|
When treating neuropathic pain in CKD 5: a) Ketamine should be used cautiously, with dose reduction. b) Gabapentin is safe to use without dose reduction. c) Tricyclics can be used cautiously. d) Pregabalin can be used but with dose reduction and a long dosing interval.
|
d
|
Palliative care for children and young people with stage 5 chronic kidney disease
|
1. An 18-year-old Caucasian male with CKD secondary to dysplastic kidneys has been on maintenance hemodialysis for over 6 years. He was noted to have valvular calcifications on recent echocardiogram but has no cardiac symptoms. At the time of the study, he was on calcium carbonate (3.5 g/d) and received calcitriol in the past for elevated PTH. Laboratory studies revealed: serum calcium, 9.4 mg/dl; phosphate, 7.6 mg/dl; and immunoreactive PTH, 230 pg/ml (normal: 10–65 pg/ml). Of the following statements about this patient’s condition, the most accurate is. a) The finding of vascular calcification can be associated with the history of hyperparathyroidism, poor control of hyperphosphatemia, and previous use of calcium-based phosphate binders. b) The echocardiogram findings more likely reflect effects of high LDL and low HDL levels than abnormalities in calcium and phosphate metabolism. c) Vascular calcifications are related to present or the previous hypoparathyroidism in children and adolescents with CKD-MBD. d) In CKD, vascular calcifications are associated with an increased risk of cardiovascular mortality later in life but not at this age.
|
a
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Pediatric CKD-MBD: existing and emerging treatment approaches
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2. You are consulted on a 10-year-old boy with newly diagnosed CKD. By history, the patient voids several times each night. On examination, he is pale. His height and weight are both below the third percentile. He has normal blood pressure and Tanner 1 pubertal development. Laboratory tests: Sodium mEq/L (mmol/L) 136 (136), Potassium mEq/L (mmol/L) 3.8 (3.8), Chloride mEq/L (mmol/L) 108 (108), Total carbon dioxide mEq/L (mmol/L) 18 (18), Serum urea nitrogen mg/dL (mmol/L) 40 (14.3), Creatinine mg/dL (µmol/L) 1.8 (159), Calcium mg/dL (mmol/L) 9.9 (2.5), Phosphorus mg/dL (mmol/L) 4.0 (1.3), Intact parathyroid hormone pg/mL (ng/L)170 (18), 25-OH-vitamin D ng/mL (nmol/L) 12 (30). The next most appropriate step in the treatment of his CKD-MBD is to initiate. a) calcitriol. b) vitamin D supplementation. c) paricalcitol. d) sevelamer carbonate.
|
b
|
Pediatric CKD-MBD: existing and emerging treatment approaches
|
3. A 16-year-old boy who has been on chronic PD for 2 years presents with lower extremity pain. He reports nonadherence with his prescribed diet, phosphate binders, and calcitriol but has not missed any dialysis treatments. His laboratory data are as follows: Laboratory test: Calcium mg/dL (mmol/L) 8.3 (2.0), Phosphorus mg/dL (mmol/L) 7.7 (2.4), Intact parathyroid hormone pg/mL (ng/L) 928 (97.7), Alkaline phosphatase IU/L (µkat/L) 345 (5.7). Based on the laboratory data, the child’s renal osteodystrophy findings could best be postulated as. a) adynamic bone. b) high bone turnover. c) low bone turnover. d) low bone volume.
|
b
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Pediatric CKD-MBD: existing and emerging treatment approaches
|
4. A 7-year-old boy on chronic PD for 2 years secondary to dysplastic kidneys presents to the clinic. When he started treatment, his height was decreased for age (height Z-score = − 2.4 SD), and his height improvement on dialysis has been minimal (Δ height Z-score = + 0.1 SD). In addition, he recently developed bilateral hip pain on ambulation and reduced exercise capacity. His medications include calcium carbonate, calcitriol, and sodium bicarbonate. His laboratory findings are as follows: Sodium mEq/L (mmol/L) 135 (135), Potassium mEq/L (mmol/L) 3.9 (3.9), Bicarbonate mEq/L (mmol/L) 16 (16), Calcium mg/dL (mmol/L) 8.5 (2.1), Phosphorus mg/dL (mmol/L) 7.4 (2.3), Serum urea nitrogen mg/dL (mmol/L) 65 (23.3), Creatinine mg/dL (µmol/L) 5 (442). Of the following, the most reliable and definitive test to assess the type and severity of his CKD-MBD is: a) bone biopsy b) combination of parathyroid hormone level and 25 hydroxyvitamin D c) serum osteocalcin and urine bone turnover markers d) 1,25 dihydroxyvitamin D level
|
a
|
Plant-based diets: a fad or the future of medical nutrition therapy for children with chronic kidney disease
|
What is the effect of the plant-based diet on bioavailability of nutrients and production of trimethylamine-N-oxide? a) Plant-based diet has increased bioavailability of protein, phosphorus, and potassium content compared to animal-based diet and decreases production of trimethylamine-N-oxide. b) Plant-based diet has increased bioavailability of protein, phosphorus, and potassium content as compared to animal-based diet and decreases production of trimethylamine-N-oxide. c) Plant-based diet has decreased bioavailability of protein, phosphorus, and potassium content compared to animal-based diet and decreases production of trimethylamine-N-oxide. d) Plant-based diet has decreased bioavailability of protein, phosphorus, and potassium content compared to animal-based diet and increases production of trimethylamine-N-oxide.
|
c
|
Plant-based diets: a fad or the future of medical nutrition therapy for children with chronic kidney disease
|
Which of the below statements regarding fat sources in plant-based diets is true? a) Fat from animal origin is high in saturated fats and low in unsaturated fats. b) Fat from plant-based diet is high in saturated fats and low in unsaturated fats. c) Vegetarian diets are high in lecithin compared to animal-based diets. d) Omega-3 and omega-6 fatty acids are types of monounsaturated fatty acids found in the plant-based diet.
|
a
|
Plant-based diets: a fad or the future of medical nutrition therapy for children with chronic kidney disease
|
Choose the best answer: a) Plant-based diet is known to help with obesity, hypertension, and dyslipidemia. b) Plant-based diet improves gut microbiota. c) Plant-based diet increases production of short-chain fatty acids. d) Fiber in the plant-based diet decreases gut motility. e) A, B, and C are true.
|
e
|
Plant-based diets: a fad or the future of medical nutrition therapy for children with chronic kidney disease
|
Which of the following options would be the best snack choice for a child with CKD: a) Packaged cheese and crackers b) Carrot sticks with homemade hummus c) Artificially fruit-flavored gummy snacks d) Baked low-sodium potato chips
|
b
|
Plant-based diets: a fad or the future of medical nutrition therapy for children with chronic kidney disease
|
Choose the best answer. Non-dairy almond milk alternative beverages: a) Are a better source of calories and protein compared to cow’s milk. b) Can be used as a plant-based substitute for breastmilk in infants with CKD. c) Is lower in potassium and phosphorus compared to cow’s milk and soy milk. d) All of the above.
|
c
|
Relationship between endothelin and nitric oxide pathways in the onset and maintenance of hypertension in children and adolescents
|
Which endothelin activates endothelinA receptors? a) Only endothelin-1 b) Only endothelin-2 c) Only endothelin-3 d) Both endothelin-1 and endothelin-2 e) Endothelin-1, endothelin-2 and endothelin-3 all activate endothelinA receptors
|
d
|
Relationship between endothelin and nitric oxide pathways in the onset and maintenance of hypertension in children and adolescents
|
Which of these substances does not stimulate the synthesis of endothelin-1? a) Thrombin b) TNF-α c) Heparin d) Insulin e) Vasopressin
|
c
|
Relationship between endothelin and nitric oxide pathways in the onset and maintenance of hypertension in children and adolescents
|
Which of these statements is incorrect? a) To be active, the nitric oxide synthase enzyme requires all these cofactors: NADH, FAD, FMN, BH4. b) The nitric oxide synthase enzyme is stimulated by endothelin-3. c) Endothelin-3 stimulates vasodilation through cyclic GMP and endothelium-derived hyperpolarizing factors. d) The nitric oxide synthase enzyme is always active in the central nervous system. e) Estrogen stimulates the production of nitric oxide synthase enzyme.
|
d
|
Relationship between endothelin and nitric oxide pathways in the onset and maintenance of hypertension in children and adolescents
|
How is endothelial dysfunction defined? a) An imbalance between vasodilating and vasoconstricting substances produced by muscle cells b) An imbalance between vasodilating and vasoconstricting substances produced by endothelial cells c) An increase in vasodilation capacity d) A decrease of pro-inflammatory and pro-thrombotic state e) An increase of nitric oxide bioavailability and a decrease of endothelin-1 plasma values
|
b
|
Relationship between endothelin and nitric oxide pathways in the onset and maintenance of hypertension in children and adolescents
|
The balance of nitric oxide and endothelin-1 in hypertensive children: a) is similar to that described in hypertensive adults b) is similar to that described in hypertensive adults only regarding the bioavailability of nitric oxide c) is influenced by the presence of excess weight d) is always characterized by an increase in plasma endothelin-1 values e) has been studied predominantly in prepubescent children and there is a lack of evidence in adolescents
|
c
|
Post-transplant education for kidney recipients and their caregivers
|
Which of the following combinations represents an age-appropriate educational strategy? A) Adolescence – focus education on caregivers to prevent loss of follow-up during transition B) Early childhood – start patient-centered education C) Middle childhood – allow time for the patient to ask independent questions D) Infancy/ Toddler – explain things simply and briefly in a way the child can understand
|
c
|
Post-transplant education for kidney recipients and their caregivers
|
Which of the following strategies has been shown to improve patient understanding of disease processes? A) Individualization of education B) Making material understandable to those with low health literacy C) Culturally competent education D) Providing resources to help patients navigate complex healthcare systems E) All of the above
|
e
|
Post-transplant education for kidney recipients and their caregivers
|
Discussion of dietary recommendations in the post-transplant period should include all but one of the following: A) Weight gain and obesity are uncommon complications after transplantation, as physical activity generally increases B) Fluid intake goals are likely to change in the post-transplant period, shifting from a restrictive to a permissive fluid goal C) Sodium may need to be restricted to prevent hypertension in the post-transplant period D) Patients should avoid taking grapefruit juice with their immunosuppressive medications
|
a
|
Post-transplant education for kidney recipients and their caregivers
|
Which of the following statements regarding post-transplant management is inaccurate? A) Live vaccines are preferred to be given prior to transplantation; however, in some situations, a risk–benefit analysis may favor post-transplant administration B) Estrogen-containing contraceptive methods have been shown to be safe in female transplant recipients and therefore can be used in any post-transplant recipient of reproductive age C) Transplant recipients should adhere to age-appropriate USPSTF STI screening recommendations at least as often as healthy children D) Most sports have a low risk of kidney injury and can be performed by transplant recipients with appropriate modifications as needed
|
b
|
Rickets guidance part II—management
|
Which of the following statements is true? a) The cause of nutritional rickets is always a deficiency of vitamin D. b) Nutritional rickets can be excluded if the 1,25(OH)2D is highly normal or even outside the upper normal range. c) Therapy of nutritional rickets is exclusively done with high vitamin D supplementation. d) During monitoring of nutritional rickets, the drop in PTH is the earliest and most important indicator of response to therapy. e) In case of tetany due to nutritional rickets, rapid initiation of vitamin D supplementation is sufficient.
|
d
|
Rickets guidance part II—management
|
Which of the following statements is true? a) The marked hypophosphatemia which may be present in nutritional rickets requires oral supplementation with phosphate salts. b) The diagnosis of vitamin D-dependent rickets type 1B should be considered if high-dose therapy with native vitamin D does not lead to a normalization of 25-OHD and a concomitant decrease in PTH levels. c) Intramuscular injection of vitamin D is the treatment of choice in nutritional rickets. d) Vitamin D-dependent rickets type 2a and 2b differ with respect to response to calcitriol therapy. e) Administration of intravenous calcium is the therapy of choice in vitamin D-dependent rickets type 1B in the first months of life.
|
b
|
Rickets guidance part II—management
|
Which of the following statements is true? a) Monitoring of children with hypophosphatemic rickets treated with phosphate salts and active vitamin D includes the assessment of serum phosphate, calcium, alkaline phosphatase, creatinine, 1,25(OH)2 vitamin D, and calculation of maximum rate of tubular reabsorption of phosphate per glomerular filtration rate (TmP/GFR). b) Children with hypophosphatemic rickets should undergo yearly X-ray examinations of the left wrist and/or lower limbs. c) Patients with hypophosphatemic rickets due to defects in sodium-dependent tubular phosphate transporters should undergo yearly hearing tests. d) Calculation of maximum rate of tubular reabsorption of phosphate per glomerular filtration rate (TmP/GFR) is recommended to assess renal phosphate wasting in children on burosumab treatment. e) Assessment of PTH levels is not helpful in the management of children with hypophosphatemic rickets treated with burosumab.
|
d
|
Rickets guidance part II—management
|
Which of the following statements is true? a) Children with hypophosphatemic rickets are usually treated with phosphate salts and active vitamin D. b) Burosumab is the treatment of choice in infants aged less than 6 months with X-linked hypophosphatemia. c) Patients with hypophosphatemic rickets due to defects in sodium-dependent tubular phosphate transporters require no treatment with active vitamin D. d) Conventional treatment with phosphate salts and active vitamin D is more effective than burosumab treatment in patients with X-linked hypophosphatemia. e) Phosphate should be given in two divided doses in patients with X-linked hypophosphatemia.
|
c
|
Rickets guidance part II—management
|
Which of the following statements is true? a) High doses of phosphate and/or active vitamin D are associated with the development of nephrocalcinosis in children with hypophosphatemic rickets. b) The starting dose of burosumab in children with X-linked hypophosphatemia amounts to 0.4 mg/kg given every two weeks subcutaneously. c) The starting dose of burosumab in children with tumor-induced osteomalacia amounts to 0.8 mg/kg given every two weeks subcutaneously. d) Active vitamin D may be combined with burosumab for treatment of X-linked hypophosphatemia. e) Burosumab should be tailored in 0.4 mg/kg increments every two weeks to raise fasting serum phosphate levels to within the lower end of the normal reference range.
|
a
|
Role of therapeutic apheresis in the treatment of pediatric kidney diseases
|
1. Which of the following statements is not correct about the principles of TPE? a) A pathogenic molecule has to be identified which is large enough to be amenable to removal only by TPE. b) Use of TPE is associated with improvement in disease. c) Pathogenic molecules are mostly distributed intracellularly. d) The half-life of the molecule should be long enough such that it does not re-accumulate quickly after TPE.
|
c
|
Role of therapeutic apheresis in the treatment of pediatric kidney diseases
|
2. Which of the following statements about TPE use in pediatric kidney disorder is false? a) TPE has been used as successful adjunctive therapy for anti-glomerular basement membrane disease that has become dialysis-dependent. b) There is not much of a role for TPE in lupus nephritis. c) TPE is used for FSGS recurrence after kidney transplant in children with other immunosuppressive therapy. d) TPE is not used in ANCA vasculitis with mild kidney disease.
|
a
|
Role of therapeutic apheresis in the treatment of pediatric kidney diseases
|
3. TPE is the standard of care in which of the following thrombotic microangiopathy (TMA)? a) TTP b) Transplantation-associated TMA c) Quinine-associated TMA d) Shiga toxin-associated HUS
|
a
|
Role of therapeutic apheresis in the treatment of pediatric kidney diseases
|
4. TPE is a useful adjunct in all the following diseases affecting kidney transplantation except? a) Antibody-mediated rejection of kidney transplant b) Cellular rejection of kidney transplant c) Recurrence of FSGS in kidney transplantation d) ABO-incompatible kidney transplantation
|
b
|
Role of therapeutic apheresis in the treatment of pediatric kidney diseases
|
5. Which of the following statements is true regarding complications associated with apheresis? a) Hypocalcemia is more common with heparin-based anticoagulation. b) The use of FFP is associated with higher rates of allergic reactions. c) Tandem TPE requires less intensive monitoring for complications. d) Critically ill children who are getting TPE are at lower risk of complications.
|
b
|
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