NEPHROLOGY (NEPH) FINAL EXAMINATION Complete
Test Bank – 100 Questions & Detailed Rationales Based
on ABIM Nephrology Board Exam Content Guidelines –
Latest 2026-2027 Edition||Practice Questions with
Verified Answers | Guaranteed Success
EXAM INSTRUCTIONS
- This final examination consists of 100 multiple-choice questions.
- Each question has four or five answer choices (A–E)**.
- Select the single best answer for each question.
- Questions are based on the BIM Nephrology Board Exam and European
Specialty Examination in Nephrology (ESENeph)** content guidelines.
- Time suggested: 2.5 hours (approximately 1.5 minutes per question).
Topics covered: Renal Physiology, Acid-Base and Electrolyte Disorders,
Glomerular Diseases, Tubulointerstitial Diseases, Acute Kidney Injury,
Chronic Kidney Disease, Dialysis, Kidney Transplantation, Hypertension,
and Mineral Bone Disorders.
,Question 1
A 45-year-old man with a history of type 2 diabetes mellitus and
hypertension is evaluated for progressively worsening kidney function. His
serum creatinine has increased from 1.2 mg/dL to 2.8 mg/dL over the past
6 months. Urinalysis reveals 3+ proteinuria and microscopic hematuria. A
kidney biopsy is performed and reveals nodular glomerulosclerosis with
mesangial expansion and thickening of the glomerular basement
membrane. Which of the following is the most likely diagnosis, and what is
the characteristic histopathological finding on electron microscopy?**
A) Minimal change disease with effacement of podocyte foot processes
B) Membranous nephropathy with subepithelial immune deposits
C) Diabetic nephropathy with diffuse and nodular mesangial expansion
(Kimmelstiel-Wilson nodules)
D) Focal segmental glomerulosclerosis (FSGS) with segmental scarring
E) IgA nephropathy with mesangial IgA deposition
Answer: C
**Rationale:** Diabetic nephropathy is characterized by thickening of the
glomerular basement membrane, mesangial expansion, and nodular
glomerulosclerosis (Kimmelstiel-Wilson nodules). These nodules are
pathognomonic for diabetic nephropathy. The patient's history of type 2
diabetes mellitus and hypertension, along with progressive proteinuria and
renal impairment, are classic features. Option A describes minimal change
disease, which is characterized by podocyte foot process effacement on
,electron microscopy and is typically seen in children with nephrotic
syndrome. Option B describes membranous nephropathy, which is
characterized by subepithelial immune deposits and is a common cause of
nephrotic syndrome in adults. Option D describes FSGS, which is
characterized by segmental scarring of the glomeruli and can be primary or
secondary. Option E describes IgA nephropathy, which is characterized by
mesangial IgA deposition and is a common cause of glomerulonephritis, but
it does not typically show nodular glomerulosclerosis.
Question 2
A 68-year-old woman with a history of hypertension and chronic kidney
disease (CKD) stage 3b is evaluated in the clinic. Her estimated glomerular
filtration rate (eGFR) is 38 mL/min/1.73 m². She has been on lisinopril 20
mg daily for blood pressure control. Her serum potassium is 5.6 mEq/L
(reference range: 3.5-5.0 mEq/L). Which of the following is the most
appropriate next step in the management of this patient's hyperkalemia?**
A) Discontinue lisinopril and start amlodipine for blood pressure control
B) Continue lisinopril and add a potassium-binding resin (sodium
polystyrene sulfonate)
C) Reduce lisinopril to 10 mg daily and monitor potassium levels in 1 week
D) Continue lisinopril and add hydrochlorothiazide to enhance potassium
excretion
, E) Discontinue lisinopril and start losartan to avoid ACE inhibitor-induced
hyperkalemia
Answer: A
Rationale: In a patient with CKD and hyperkalemia (potassium > 5.5 mEq/L)
on an ACE inhibitor (lisinopril), the most appropriate management is to
discontinue the ACE inhibitor and consider alternative antihypertensive
agents such as amlodipine. ACE inhibitors and ARBs reduce aldosterone
secretion, leading to decreased potassium excretion and hyperkalemia,
particularly in patients with CKD. Option B is incorrect because while
potassium-binding resins can be used for acute management, the
underlying cause (ACE inhibitor) should be addressed. Option C is incorrect
because dose reduction may not adequately resolve hyperkalemia, and the
patient is already on a moderate dose. Option D is incorrect because adding
a thiazide diuretic may worsen renal function and does not address the
mechanism of hyperkalemia. Option E is incorrect because ARBs also cause
hyperkalemia; switching from an ACE inhibitor to an ARB does not resolve
the issue.
Test Bank – 100 Questions & Detailed Rationales Based
on ABIM Nephrology Board Exam Content Guidelines –
Latest 2026-2027 Edition||Practice Questions with
Verified Answers | Guaranteed Success
EXAM INSTRUCTIONS
- This final examination consists of 100 multiple-choice questions.
- Each question has four or five answer choices (A–E)**.
- Select the single best answer for each question.
- Questions are based on the BIM Nephrology Board Exam and European
Specialty Examination in Nephrology (ESENeph)** content guidelines.
- Time suggested: 2.5 hours (approximately 1.5 minutes per question).
Topics covered: Renal Physiology, Acid-Base and Electrolyte Disorders,
Glomerular Diseases, Tubulointerstitial Diseases, Acute Kidney Injury,
Chronic Kidney Disease, Dialysis, Kidney Transplantation, Hypertension,
and Mineral Bone Disorders.
,Question 1
A 45-year-old man with a history of type 2 diabetes mellitus and
hypertension is evaluated for progressively worsening kidney function. His
serum creatinine has increased from 1.2 mg/dL to 2.8 mg/dL over the past
6 months. Urinalysis reveals 3+ proteinuria and microscopic hematuria. A
kidney biopsy is performed and reveals nodular glomerulosclerosis with
mesangial expansion and thickening of the glomerular basement
membrane. Which of the following is the most likely diagnosis, and what is
the characteristic histopathological finding on electron microscopy?**
A) Minimal change disease with effacement of podocyte foot processes
B) Membranous nephropathy with subepithelial immune deposits
C) Diabetic nephropathy with diffuse and nodular mesangial expansion
(Kimmelstiel-Wilson nodules)
D) Focal segmental glomerulosclerosis (FSGS) with segmental scarring
E) IgA nephropathy with mesangial IgA deposition
Answer: C
**Rationale:** Diabetic nephropathy is characterized by thickening of the
glomerular basement membrane, mesangial expansion, and nodular
glomerulosclerosis (Kimmelstiel-Wilson nodules). These nodules are
pathognomonic for diabetic nephropathy. The patient's history of type 2
diabetes mellitus and hypertension, along with progressive proteinuria and
renal impairment, are classic features. Option A describes minimal change
disease, which is characterized by podocyte foot process effacement on
,electron microscopy and is typically seen in children with nephrotic
syndrome. Option B describes membranous nephropathy, which is
characterized by subepithelial immune deposits and is a common cause of
nephrotic syndrome in adults. Option D describes FSGS, which is
characterized by segmental scarring of the glomeruli and can be primary or
secondary. Option E describes IgA nephropathy, which is characterized by
mesangial IgA deposition and is a common cause of glomerulonephritis, but
it does not typically show nodular glomerulosclerosis.
Question 2
A 68-year-old woman with a history of hypertension and chronic kidney
disease (CKD) stage 3b is evaluated in the clinic. Her estimated glomerular
filtration rate (eGFR) is 38 mL/min/1.73 m². She has been on lisinopril 20
mg daily for blood pressure control. Her serum potassium is 5.6 mEq/L
(reference range: 3.5-5.0 mEq/L). Which of the following is the most
appropriate next step in the management of this patient's hyperkalemia?**
A) Discontinue lisinopril and start amlodipine for blood pressure control
B) Continue lisinopril and add a potassium-binding resin (sodium
polystyrene sulfonate)
C) Reduce lisinopril to 10 mg daily and monitor potassium levels in 1 week
D) Continue lisinopril and add hydrochlorothiazide to enhance potassium
excretion
, E) Discontinue lisinopril and start losartan to avoid ACE inhibitor-induced
hyperkalemia
Answer: A
Rationale: In a patient with CKD and hyperkalemia (potassium > 5.5 mEq/L)
on an ACE inhibitor (lisinopril), the most appropriate management is to
discontinue the ACE inhibitor and consider alternative antihypertensive
agents such as amlodipine. ACE inhibitors and ARBs reduce aldosterone
secretion, leading to decreased potassium excretion and hyperkalemia,
particularly in patients with CKD. Option B is incorrect because while
potassium-binding resins can be used for acute management, the
underlying cause (ACE inhibitor) should be addressed. Option C is incorrect
because dose reduction may not adequately resolve hyperkalemia, and the
patient is already on a moderate dose. Option D is incorrect because adding
a thiazide diuretic may worsen renal function and does not address the
mechanism of hyperkalemia. Option E is incorrect because ARBs also cause
hyperkalemia; switching from an ACE inhibitor to an ARB does not resolve
the issue.
