The NephroTube CKD Module End Exam assesses advanced knowledge in managing chronic kidney disease (CKD) related to various conditions. It evaluates understanding of treatment protocols, disease progression, and patient management, crucial for medical professionals specializing in nephrology and internal medicine.
She does not have chronic kidney disease (CKD) because her serum creatinine and protein excretion are both normal.
Estimating glomerular filtration rate (GFR) using the Modification of Diet in Renal Disease (MDRD) study equation is not accurate in PKD patients.
She has CKD on the basis of the microscopic hematuria and abnormal renal ultrasound.
On the basis of her current serum creatinine, she is unlikely to develop ESRD during her lifetime.
GFR should be measured by 125I-iothalamate clearance to appropriately stage her CKD.
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She should be advised to lower her salt intake with follow-up blood pressure (BP) and serum creatinine in 4 mo.
She should be referred for laparoscopic deroofing of her renal cysts.
Anti-hypertensive therapy should be started with a thiazide diuretic, and a beta-blocker could be added if needed.
She should be placed on dietary protein restriction (0.6 g/kg per d).
She should be treated with an angiotensinconverting enzyme (ACE) inhibitor to a target BP of 130/85 mmHg.
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The Cockcroft-Gault equation is more accurate than the MDRD equation for estimating GFR in patients 70-yr-old.
A kidney biopsy is indicated to define the underlying renal pathology.
On the basis of the urinary protein excretion rate and GFR, he has stage 3 chronic kidney disease (CKD).
The low GFR is a consequence of aging, and he should not be classified as having CKD.
The thiazide diuretic should be switched to a loop diuretic.
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White patients have a higher risk of progression compared with patients from other ethnic groups.
Few glomeruli were globally sclerosed; therefore, her renal prognosis is good.
The severity of tubulointerstitial disease is a good predictor of kidney disease progression.
Proteinuria is not a risk factor for kidney disease progression.
On the basis of the amount of proteinuria, she is unlikely to respond to an angiotensinconverting enzyme (ACE) inhibitor.
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Hematocrit is a more accurate way of defining anemia than hemoglobin.
Erythropoietin levels are useful in deciding treatment.
A bone marrow biopsy should be performed to rule out myelodysplastic syndrome.
Serum iron, transferrin saturation, and ferritin should be measured to assess iron stores.
Proteinuria is associated with a poor response to erythropoietin therapy.
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Treatment of anemia is associated with higher rates of hospitalizations.
Treatment of anemia can prevent the development of left ventricular hypertrophy.
Erythropoietin can accelerate the progression of kidney disease.
Treatment with recombinant erythropoietin should only be initiated when the hemoglobin is 8 g/dl.
Target hemoglobin levels with recombinant erythropoietin should be 11 g/dl.
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At this stage in his kidney disease, glycemic control is likely to be beneficial in slowing the progression.
He has a low risk of kidney disease progression.
His target BP should not be lowered because it would increase his risk of sudden cardiac death (J point phenomenon).
Addition of an angiotensin receptor blocker will further decrease the progression of his kidney disease.
Lowering his target BP can slow the progression of his kidney disease.
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Carefully follow his hemoglobin and start recombinant erythropoietin therapy if it decreased to 8 g/dl.
Check an echocardiogram and start recombinant erythropoietin therapy if left ventricular hypertrophy is present.
Start oral iron and recheck hemoglobin level in 1 mo.
Start recombinant erythropoietin 10,000 units subcutaneously once weekly along with oral iron.
Transfuse 2 units of packed red blood cells.
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Dietary phosphorus should be restricted to 2 g/d.
He should be treated with 0.25 g/d calcitriol.
Calcium-containing phosphate binders should be avoided.
Long-term therapy with aluminum hydroxide should be started at a dose of 15 ml orally with meals.
Sevelamer therapy would be associated with an increased risk of development of osteomalacia and bone fractures.
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Anti-hypertensive therapy is not indicated because she is normotensive, but she should have BP monitored every 3 mo.
Therapy should be started with a dihydropyridine calcium channel blocker to prevent the development of diabetic nephropathy.
Anti-hypertensive therapy is not indicated at the present time, but an angiotensin-converting enzyme (ACE) inhibitor should be started if her urinary albumin-to-creatinine ratio increases to 355 mg/g.
ACE inhibitors have been demonstrated to reduce albuminuria and decrease the risk of progressing to overt diabetic nephropathy.
Angiotensin receptor blockers have been demonstrated to reduce albuminuria and reduce the risk of progressing to overt diabetic nephropathy.
Continue on his present treatment and return when his serum creatinine is 6 mg/ dl.
Once he starts on dialysis, he should be evaluated as a kidney transplant candidate.
Vascular access for dialysis should be placed in preparation for needed dialysis.
Preemptive living donor transplant if a donor is available.
Start on a low-protein diet of 0.3 g/kg per d to delay the need for dialysis.
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No adverse effects of acidosis are seen until the bicarbonate is 15 mEq/L.
Acidosis stimulates albumin synthesis by the liver.
Acidosis suppresses parathyroid hormone release.
Acidosis increases calcium loss from bone.
Acidosis stimulates skeletal muscle hypertrophy.
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The most sensitive marker of abnormal mineral metabolism is decreased calcitriol production.
Elevations in parathyroid hormone (PTH) secretion do not occur until GFR is 20 ml/min per 1.73 m2.
Elevated serum phosphorus inhibits the 1-alpha hydroxylase enzyme in the kidney, leading to decreased calcitriol synthesis.
An alteration in the set point for calcium occurs in the parathyroid glands, leading to increased PTH secretion for any increase in serum calcium.
The most common bone abnormality is osteomalacia.
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The percentage of glomeruli with focal changes on biopsy.
Angiotensin-converting enzyme (ACE) genotyping for polymorphisms.
The extent of tubulointerstitial disease on biopsy.
The level of plasma renin activity.
A family history of hypertension.
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Microalbuminuria is not a risk factor for cardiovascular disease.
Most patients with chronic kidney disease will die of cardiovascular disease before they reach end stage renal disease.
CKD is a risk factor for coronary artery disease but not for stroke or peripheral vascular disease.
CKD is a risk factor for cardiovascular disease only when the serum creatinine is 3 mg/dl.
A higher prevalence of traditional risk factors such as hypertension and dyslipidemia account for the increased risk of cardiovascular disease in patients with CKD.
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The patient has nephrotic range proteinuria.
There is contradictory information presented regarding whether or not patient has nephrotic range proteinuria.
There is insufficient information to determine whether or not the patient has nephrotic range proteinuria.
The random spot urine protein/creatinine ratio is misleading because of the low creatinine production.
It is not valid to use urine protein/creatinine ratio to assess proteinuria when the serum albumin level is low.
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Stage 1.
Stage 2.
Stage 3.
Stage 4.
Stage 5.
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The patient’s baseline CKD is unrelated to his acute renal failure.
Intravenous contrast is not contraindicated in patients with CKD.
The patient’s diabetes is not a risk factor for his acute renal failure.
The patient’s GFR when his creatinine rose to 2.4 mg/dl is approximately 30 ml/ min/1.73m2.
To measure the patient’s current creatinine clearance, a 24-h urine collection should be started the morning when his serum creatinine rose to 2.4 mg/dl.
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Iron deficiency
Malignancy
Trauma
Drugs
PRCA
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