Nephrology — MCQs

A 29-year-old male with HIV, on indinavir, zidovudine, and stavudine, presents with severe edema and a serum creatinine of 2.0 mg/dL. He has had bone pain for 5 years and takes large amounts of acetaminophen with codeine, aspirin, and ibuprofen. He is on prophylactic trimethoprim-sulfamethoxazole. Blood pressure is 170/110; urinalysis shows 4+ protein, 5 to 10 RBCs; 24-hour urine protein is 6.2 g. What is the most likely cause of his renal disease?

Nephrology Indian Medical PG Practice Questions and MCQs

Question 861: What is the term for the triad of renal colic, loin swelling that resolves after urination?

A. Kocher's triad
B. Saint's triad
C. Dietel's crisis (Correct Answer)
D. Charcot's triad

Explanation: ***Dietel's crisis*** * It is characterized by recurrent attacks of **renal colic**, **loin swelling** (due to hydronephrosis), and hematuria, which resolve after increased urine output [1]. * This triad is typically associated with **intermittent ureteropelvic junction (UPJ) obstruction**, where urine outflow is temporarily blocked [1]. *Kocher's triad* * This triad refers to the classic symptoms of acute appendicitis: **pain shifting from the periumbilical region to the right iliac fossa**, **anorexia**, and **nausea/vomiting**. * It is not related to renal issues or loin swelling. *Saint's triad* * This triad describes the coexistence of **gallstones**, **diverticulosis**, and **hiatal hernia**. * It represents three common conditions often found together in older adults but has no connection to kidney problems. *Charcot's triad* * This triad is composed of **jaundice**, **right upper quadrant pain**, and **fever**, which are indicative of acute cholangitis. * It is entirely distinct from renal colic and loin swelling.

Question 862: What is the most common initial presentation of Alport's syndrome?

A. AR inheritance
B. End-stage renal disease
C. Lenticonus
D. Hematuria (Correct Answer)

Explanation: ### Hematuria - This is the most consistent and often the earliest clinical manifestation of **Alport's syndrome**, appearing in nearly all affected individuals [1]. - **Microscopic hematuria** is typically present from childhood due to structural abnormalities in the **glomerular basement membrane (GBM)** [1]. ### Lenticonus - While **lenticonus** (conical protrusion of the lens) is a characteristic ocular manifestation of Alport's syndrome, it is not an initial or common presentation. - It usually develops later in life and is not a universal finding, unlike hematuria. ### AR inheritance - This option describes an **inheritance pattern** (autosomal recessive) and not a clinical presentation. - The most common inheritance pattern for Alport's syndrome is **X-linked (COL4A5 gene)**, affecting males more severely. ### End-stage renal disease - **End-stage renal disease (ESRD)** is a serious complication and the natural progression of Alport's syndrome, but it is not the initial presentation. - ESRD typically develops in late adolescence or early adulthood, following years of progressive renal damage [2].

Question 863: In the oliguric phase of renal failure, which of the following statements is false?

A. Anaemia
B. Hyperkalemia
C. Hyponatremia
D. Hypercalcemia (Correct Answer)

Explanation: ### Hypercalcemia - In the oliguric phase of renal failure, **hypercalcemia** is typically *not* seen; rather, **hypocalcemia** is common due to impaired vitamin D activation and phosphate retention [1]. - The kidneys are crucial for activating vitamin D, which helps regulate **calcium absorption**. With renal failure, this activation is impaired [1]. *Hyponatremia* - **Hyponatremia** is common in the oliguric phase due to fluid overload and the kidneys' inability to excrete excess water, diluting serum sodium concentrations. - Patients accumulate fluid, leading to **dilutional hyponatremia**. *Anaemia* - **Anemia** is a frequent complication of renal failure, primarily due to decreased production of **erythropoietin** by the damaged kidneys [1]. - Reduced erythropoietin production impairs red blood cell formation in the bone marrow [1]. *Hyperkalemia* - **Hyperkalemia** is a significant concern in the oliguric phase because the kidneys are unable to adequately excrete potassium [1]. - Potassium accumulation can lead to life-threatening **cardiac arrhythmias**.

Question 864: Which type of nephrotic syndrome is most commonly associated with malaria?

A. Membranoproliferative glomerulonephritis (MPGN)
B. Minimal change disease (MCD) (Correct Answer)
C. Membranous nephropathy
D. Focal segmental glomerulosclerosis (FSGS)

Explanation: Minimal change disease (MCD) - While various nephropathies can be associated with malaria, minimal change disease is most commonly reported, particularly in children living in endemic areas. [1] - The exact mechanism is unclear but may involve altered T-cell function or cytokine production triggered by malarial infection leading to podocyte dysfunction. [1] Membranoproliferative glomerulonephritis (MPGN) - MPGN is more commonly associated with chronic infections like Hepatitis C and certain autoimmune diseases, rather than acute or chronic malaria as the primary cause of nephrotic syndrome. - While chronic parasitic infections can sometimes be linked to MPGN, it is not the most frequent cause of nephrotic syndrome in the context of malaria. Membranous nephropathy - This condition is often associated with Hepatitis B, syphilis, or certain malignancies, and autoimmune diseases. - It is not the most prevalent form of nephrotic syndrome directly attributed to malarial infection. Focal segmental glomerulosclerosis (FSGS) - FSGS has a wide range of etiologies, including HIV infection, drug-induced causes, and genetic mutations. [1] - Although it can be secondary to various insults, it is not the most common form of nephrotic syndrome seen specifically with malaria.

Question 865: A patient with chronic kidney disease is experiencing prolonged vomiting episodes. Given the patient's arterial blood gas (ABG) results showing a pH of 7.42, a pCO2 of 40 mmHg, and a bicarbonate level of 25 mmol/L, what is the most likely acid-base disturbance?

A. Metabolic acidosis and metabolic alkalosis (Correct Answer)
B. Metabolic acidosis and respiratory acidosis
C. Metabolic acidosis and compensated respiratory alkalosis
D. Normal ABG repo with normal electrolytes

Explanation: Metabolic acidosis and metabolic alkalosis - The ABG values of **pH 7.42**, **pCO2 40 mmHg**, and **bicarbonate 25 mmol/L** appear normal, but this patient has **chronic kidney disease (CKD)** which predisposes to **metabolic acidosis** [3], and **prolonged vomiting** which causes **metabolic alkalosis** [1]. - The normal pH, pCO2, and bicarbonate with concurrent severe metabolic acidosis and alkalosis suggest a **mixed acid-base disorder** where one disturbance is counteracting the other, resulting in a near-normal ABG [5]. Metabolic acidosis and respiratory acidosis - **Chronic kidney disease** can lead to **metabolic acidosis** [3], but prolonged **vomiting** typically causes **metabolic alkalosis**, not acidosis [1]. - There are no signs of **respiratory acidosis** (e.g., elevated pCO2) in the provided ABG results [4]. Metabolic acidosis and compensated respiratory alkalosis - While **CKD** can cause **metabolic acidosis**, prolonged **vomiting** would cause **metabolic alkalosis**, not induce a **respiratory alkalosis** [1]. - A compensated respiratory alkalosis would typically show a **lower pCO2** than 40 mmHg [2]. Normal ABG repo with normal electrolytes - Although the provided ABG values are within the normal range, the patient's underlying conditions of **chronic kidney disease** and **prolonged vomiting** are strong indicators of significant acid-base imbalances. - **CKD** inherently makes proper acid-base regulation difficult, and **vomiting** directly impacts electrolyte and acid-base balance, making a truly normal state unlikely [1][5].

Question 866: The most common form of acute kidney injury is:

A. Prerenal azotemia (Correct Answer)
B. Acute tubular injury
C. Acute interstitial nephritis
D. Acute glomerular disease

Explanation: ***Prerenal azotemia*** - This is the most prevalent form of **acute kidney injury (AKI)**, accounting for approximately 50-60% of all cases [1]. - It results from **decreased renal perfusion**, leading to reduced glomerular filtration without direct damage to the kidney parenchyma [1]. *Acute tubular injury* - This is an **intrinsic form of AKI** characterized by damage to the renal tubules, often due to ischemia or nephrotoxins [1]. - While common, it is usually a consequence of prolonged or severe prerenal AKI, and thus not the *most* common initial cause [1]. *Acute interstitial nephritis* - This involves inflammation of the kidney's **interstitial tissue**, often triggered by **allergic reactions to medications** or infections [2]. - It represents a smaller percentage of AKI cases compared to prerenal causes. *Acute glomerular disease* - This form of AKI involves direct injury to the **glomeruli**, such as in glomerulonephritis [2]. - While serious, glomerular diseases are significantly less common as a cause of overall AKI compared to prerenal factors.

Question 867: In a case of hematuria of glomerular origin, urine examination shows the presence of all of the following except:

A. Dysmorphic red cells
B. Crenated red cells
C. Red cell casts
D. Acanthocytes (Correct Answer)

Explanation: ***Acanthocytes*** - Acanthocytes, or "spur cells," are **abnormally shaped red blood cells with thorny projections**. While they can be seen in some renal diseases (e.g., end-stage renal disease), their presence is **not a defining characteristic or a specific marker of glomerular hematuria**. [1] - Glomerular hematuria is primarily characterized by features indicating red blood cell passage through a damaged glomerular basement membrane. *Crenated red cells* - **Crenated red cells** appear shrunken with thorny or scalloped borders due to water loss in hypertonic urine. [1] - While they can be seen in a urine sample, their presence **does not specifically indicate a glomerular origin** of hematuria as they form due to osmotic changes in the urine environment, not passage through a damaged glomerulus. [1] *Dysmorphic red cells* - **Dysmorphic red cells** are red blood cells that have undergone structural changes, such as blebbing or budding, as they pass through the damaged glomerular basement membrane. - Their presence is a **strong indicator of glomerular hematuria**, suggesting that the blood originates from the kidney's filtering units. [1] *Red cell casts* - **Red cell casts** are cylindrical structures formed in the renal tubules, composed of red blood cells embedded in a protein (Tamm-Horsfall) matrix. - They are considered **pathognomonic for glomerular bleeding or acute glomerulonephritis**, as they can only form when red blood cells enter the tubules from the glomeruli. [1]

Question 868: All of the following statements about hyponatremia are true, except:

A. NSAIDs increase the potency of vasopressin
B. Hyponatremia associated with hyperglycemia has high plasma osmolality
C. Hyponatremia associated with SIADH is normovolemic
D. Pseudohyponatremia is associated with low plasma osmolality (Correct Answer)

Explanation: ***Pseudohyponatremia is associated with low plasma osmolality*** - **Pseudohyponatremia** is an artifact caused by very high levels of plasma proteins or lipids, which interfere with the measurement of sodium. - In pseudohyponatremia, the actual measured **plasma osmolality** is normal because it is largely determined by the effective osmoles like sodium, glucose, and urea, which are not truly diluted in this condition [2]. *Hyponatremia associated with hyperglycemia has high plasma osmolality* - **Hyperglycemia** leads to an osmotic shift of water from the intracellular to the extracellular space, diluting serum sodium concentration. - Despite the diluted sodium, the high glucose levels contribute significantly to plasma osmolality, resulting in a **high plasma osmolality** [1]. *Hyponatremia associated with SIADH is normovolemic* - In **SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion)**, there is excessive secretion of ADH, leading to increased water reabsorption in the kidneys. - This results in dilutional hyponatremia, and the body's **effective circulating volume** remains normal or slightly increased, classifying it as euvolemic or normovolemic hyponatremia [3]. *NSAIDs increase the potency of vasopressin* - **NSAIDs** can potentiate the action of **vasopressin (ADH)** by inhibiting prostaglandin synthesis in the kidneys [4]. - Prostaglandins normally antagonize ADH's effect on water reabsorption; therefore, their inhibition leads to increased water retention and can worsen or contribute to hyponatremia.

Question 869: ANCA is sensitive and specific for which condition?

A. Post streptococcal glomerulonephritis
B. Diffuse glomerulosclerosis
C. Henoch's Schönlein-Purpura
D. ANCA-associated crescentic glomerulonephritis (Correct Answer)

Explanation: ***ANCA-associated crescentic glomerulonephritis*** - **ANCA (Anti-neutrophil cytoplasmic antibodies)** are highly sensitive and specific for various **vasculitides** that often manifest as **rapidly progressive glomerulonephritis (RPGN)**, also known as crescentic glomerulonephritis [1]. - The presence of ANCA, particularly **p-ANCA (MPO-ANCA)** or **c-ANCA (PR3-ANCA)**, is a diagnostic hallmark of conditions like **granulomatosis with polyangiitis (Wegener's)**, **microscopic polyangiitis**, and **eosinophilic granulomatosis with polyangiitis (Churg-Strauss)**, all of which can cause crescentic glomerulonephritis [1]. *Post-streptococcal glomerulonephritis* - This condition is typically characterized by a **recent streptococcal infection** and is associated with **low C3 complement levels** and **anti-streptolysin O (ASO) titers**, not ANCA [2]. - Renal biopsy often shows **subepithelial humps** on electron microscopy and **C3 deposition**, which is distinct from ANCA-associated glomerulonephritis [2]. *Diffuse glomerulosclerosis* - This is a general term for widespread scarring of the glomeruli, which can result from various chronic conditions like **diabetes** or **hypertension**. - It is a morphological finding rather than a specific disease entity and is not directly associated with ANCA. *Henoch's Schönlein-Purpura* - This is an **IgA vasculitis** primarily affecting small vessels, characterized by a rash, arthralgia, abdominal pain, and kidney involvement (IgA nephropathy) [3]. - It is associated with **IgA deposits** in affected tissues, not ANCA [3].

Question 870: A 29-year-old male with HIV, on indinavir, zidovudine, and stavudine, presents with severe edema and a serum creatinine of 2.0 mg/dL. He has had bone pain for 5 years and takes large amounts of acetaminophen with codeine, aspirin, and ibuprofen. He is on prophylactic trimethoprim-sulfamethoxazole. Blood pressure is 170/110; urinalysis shows 4+ protein, 5 to 10 RBCs; 24-hour urine protein is 6.2 g. What is the most likely cause of his renal disease?

A. Analgesic nephropathy
B. Indinavir toxicity
C. Focal sclerosis (Correct Answer)
D. Trimethoprim-sulfamethoxazole-induced interstitial nephritis

Explanation: Focal sclerosis - The combination of **HIV infection**, severe **proteinuria** (>3.5g/day, here 6.2g/day), and **hypertension** in an African American male strongly suggests **HIV-associated nephropathy (HIVAN)**, which often manifests as focal segmental glomerulosclerosis (FSGS) on biopsy [2]. - **HIVAN** is characterized by rapidly progressive renal failure, heavy proteinuria, and is more common in individuals of African descent [2]. *Indinavir toxicity* - **Indinavir** is a protease inhibitor known to cause **nephrolithiasis** (kidney stones) and **crystal-induced nephropathy**, presenting with acute kidney injury. - It typically does not cause the severe, sustained proteinuria seen in this patient, which is characteristic of glomerular disease [1]. *Analgesic nephropathy* - This condition is caused by chronic overuse of **NSAIDs and acetaminophen**, leading to **papillary necrosis** and **chronic interstitial nephritis**. - While the patient uses these medications, his primary presentation of heavy proteinuria and rapid decline in renal function points away from typical analgesic nephropathy, which usually involves milder proteinuria and sterile pyuria [1]. *Trimethoprim-sulfamethoxazole-induced interstitial nephritis* - هذا الدواء يمكن أن يسبب **التهاب الكلى الخلالي الحاد (AIN)**، والذي يترافق عادةً مع **حمى، طفح جلدي، فرط الحمضات (Eosinophilia)**، وارتفاع في الكرياتينين [1]. - While it can cause renal dysfunction, it is less likely to cause the severe proteinuria (6.2 g) observed in this patient, which is more indicative of a glomerular lesion [1].

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Acute Kidney Injury

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Chronic Kidney Disease

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Glomerular Diseases

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Tubulointerstitial Diseases

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Nephrotic and Nephritic Syndromes

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Urinary Tract Infections

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Renal Replacement Therapy

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Fluid and Electrolyte Disorders

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Acid-Base Disorders

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Kidney in Systemic Diseases

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Kidney Stones and Obstructive Uropathy

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Hypertension in Kidney Disease

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Nephrology — MCQs

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