Nephrology — MCQs
On this page
Abnormality in Renal tubular acidosis with rickets is:
A 14-year-old boy presents to the hospital with severe leg swelling that started 2 weeks ago. He also notes feeling tired and having little energy to play sports with his friends. His past medical history is negative and he is not taking any medications. On examination, his blood pressure is 163/96 mm Hg, and there is pedal edema up to his knees, as well as periorbital edema. His remaining clinical exam is normal. A urinalysis is positive for 3+ proteinuria and on 24-hour urine collection the total protein excretion is 5.4 grams/day. He undergoes a renal biopsy and there are no changes seen on light microscopy, but electron microscopy shows foot process fusion and no deposits on the membranes. Which of the following is the most likely diagnosis?
Most common nephropathy in world is?
All of the following are true about anemia of chronic kidney disease except
A 9-year-old boy is brought with history of decreased urine output, cola colored urine and swelling of the face and hands, of 2 days duration. He is hypertensive, has a puffy face and pitting edema of the lower limbs. He has history of skin lesions 4 weeks earlier. A diagnosis of post streptococcal glomerulonephritis is made. ASO titers are likely to be?
A 40-year-old man has been diagnosed with autosomal dominant polycystic kidney disease. How should the cysts be present in USG to call it ADPKD?
Dialysis patients are prone to develop
Microscopic Hematuria is defined as:
Autosomal recessive Polycystic kidneys - all are true except -
Acute hyponatremia in an 8-month-old infant may produce all except:
Nephrology Indian Medical PG Practice Questions and MCQs
Question 671: Abnormality in Renal tubular acidosis with rickets is:
- A. Loss of K+
- B. Loss of Ca2+
- C. Loss of HCO3
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Renal Tubular Acidosis (RTA)** can lead to several electrolyte abnormalities, and when complicated by **rickets**, it implies a significant impact on mineral metabolism [1], [2]. - In most forms of RTA, especially **Type 1 (distal RTA)** and **Type 2 (proximal RTA)**, there is an impairment in either **bicarbonate reabsorption** (proximal) or **hydrogen ion secretion** (distal), leading to **metabolic acidosis** [1]. This chronic acidosis contributes to bone demineralization (rickets in children, osteomalacia in adults) through various mechanisms, including increased bone resorption and decreased calcium reabsorption [2]. *Loss of K+* - **Type 1 (distal) RTA** is often associated with **hypokalemia** due to increased potassium excretion from the collecting duct in an attempt to excrete H+ ions or increased flow rates. - While not universally present in all RTA types, significant **potassium wasting** can occur, exacerbating overall electrolyte imbalance. *Loss of Ca2+* - In many forms of RTA, the **chronic metabolic acidosis** leads to increased **calcium mobilization from bone** and **impaired renal calcium reabsorption**. - This results in **hypercalciuria** (excessive calcium in urine) and **hypocalcemia**, which directly contribute to the development and severity of **rickets** (in children) or **osteomalacia** (in adults) [2]. *Loss of HCO3* - The fundamental defect in all forms of RTA is an inability of the kidneys to appropriately **reabsorb bicarbonate** or **excrete hydrogen ions**, leading to **metabolic acidosis** [1]. - Specifically, proximal RTA involves defective **bicarbonate reabsorption** in the proximal tubule, while distal RTA involves defective **hydrogen ion secretion** in the collecting duct, both resulting in a net loss or inability to conserve **bicarbonate** [1].
Question 672: A 14-year-old boy presents to the hospital with severe leg swelling that started 2 weeks ago. He also notes feeling tired and having little energy to play sports with his friends. His past medical history is negative and he is not taking any medications. On examination, his blood pressure is 163/96 mm Hg, and there is pedal edema up to his knees, as well as periorbital edema. His remaining clinical exam is normal. A urinalysis is positive for 3+ proteinuria and on 24-hour urine collection the total protein excretion is 5.4 grams/day. He undergoes a renal biopsy and there are no changes seen on light microscopy, but electron microscopy shows foot process fusion and no deposits on the membranes. Which of the following is the most likely diagnosis?
- A. membranous glomerulonephritis
- B. focal glomerulosclerosis
- C. minimal change disease (Correct Answer)
- D. mesangial proliferative glomerulonephritis
Explanation: ***minimal change disease*** - This diagnosis is strongly supported by the patient's age (child/adolescent), presentation with **nephrotic syndrome** (edema, severe proteinuria), and characteristic renal biopsy findings of **foot process fusion** on electron microscopy with **no changes on light microscopy**. [1] - **Minimal change disease** is the most common cause of nephrotic syndrome in children and typically presents with sudden onset of edema and significant proteinuria without hematuria or other signs of inflammation. [1], [2] *membranous glomerulonephritis* - This condition typically presents with **nephrotic syndrome** but is more common in adults and usually shows **thickening of the glomerular basement membrane** with subepithelial deposits on electron microscopy, which were not seen in this case. - Light microscopy in membranous glomerulonephritis often reveals diffuse capillary wall thickening, which is absent here. *focal glomerulosclerosis* - While **focal segmental glomerulosclerosis (FSGS)** can cause nephrotic syndrome and foot process effacement, light microscopy would show **sclerosis in segments of some glomeruli**, which is not described. [2] - FSGS is often characterized by the presence of **scarring** in the glomeruli, which is absent in this patient's biopsy report. [3] *mesangial proliferative glomerulonephritis* - This would show **proliferation of mesangial cells** on light microscopy, often associated with mesangial immune deposits, which is not consistent with the "no changes seen on light microscopy" finding. - This condition frequently presents with **hematuria** in addition to proteinuria, which is not mentioned in the patient's symptoms.
Question 673: Most common nephropathy in world is?
- A. FSGS
- B. IgA nephropathy (Correct Answer)
- C. Minimal Change ds
- D. Adult PSGN
Explanation: ***IgA nephropathy*** - **IgA nephropathy**, also known as **Berger's disease**, is the most common cause of primary glomerulonephritis worldwide [1]. - It is characterized by the deposition of **IgA immune complexes** in the glomeruli [1]. *FSGS* - **Focal segmental glomerulosclerosis (FSGS)** is a significant cause of nephrotic syndrome but is not the most common primary glomerulonephritis overall [1]. - It is more prevalent in certain populations and is a leading cause of **end-stage renal disease**. *Minimal Change ds* - **Minimal change disease** is the most common cause of nephrotic syndrome in children but is less common in adults and overall [1]. - It typically presents with **nephrotic range proteinuria** and a characteristic foot process effacement on electron microscopy. *Adult PSGN* - **Post-streptococcal glomerulonephritis (PSGN)** typically occurs after a streptococcal infection and is acute, not the most common chronic nephropathy [1]. - While it can occur in adults, it is far more common in children and is characterized by a latency period after infection [1].
Question 674: All of the following are true about anemia of chronic kidney disease except
- A. Normocytic normochromic anemia
- B. Dialysis worsens anemia of renal failure
- C. Erythropoietin improves the symptom
- D. Anemia is proportional to the kidney disease (Correct Answer)
Explanation: ***Anemia is proportional to the kidney disease*** - While anemia is a common complication of **CKD**, its severity doesn't always directly correlate with the degree of **kidney function decline** [1]. - Other factors like **inflammation**, **iron deficiency**, and **dialysis-related blood loss** can independently influence the severity of anemia, sometimes disproportionately [2]. *Normocytic normochromic anemia* - **Anemia of chronic kidney disease (CKD)** is typically a **normocytic normochromic anemia**, meaning the red blood cells are normal in size (normocytic) and hemoglobin content (normochromic). - This is primarily due to the **reduced production of erythropoietin** by the kidneys [3]. *Dialysis worsens anemia of renal failure* - **Dialysis** can indeed worsen anemia in patients with renal failure due to several factors including **blood loss during the dialysis procedure**, residual blood in the dialyzer, and increased **hepcidin levels** leading to **iron sequestration** [2], [3]. - Additionally, hemodialysis can induce **inflammation**, which further contributes to **hyporesponsiveness to erythropoietin**. *Erythropoietin improves the symptom* - **Erythropoietin-stimulating agents (ESAs)** are a cornerstone of treatment for anemia of CKD, as they replace the deficient **endogenous erythropoietin** and stimulate red blood cell production [3]. - While ESAs improve **hemoglobin levels** and consequently the symptoms associated with anemia, they do not cure the underlying kidney disease or address all aspects of anemia management, such as **iron deficiency** [3].
Question 675: A 9-year-old boy is brought with history of decreased urine output, cola colored urine and swelling of the face and hands, of 2 days duration. He is hypertensive, has a puffy face and pitting edema of the lower limbs. He has history of skin lesions 4 weeks earlier. A diagnosis of post streptococcal glomerulonephritis is made. ASO titers are likely to be?
- A. Not elevated (Correct Answer)
- B. Initially elevated, rapidly fall in 3-4 days
- C. Elevated
- D. Increased progressively over 2 weeks
Explanation: ***Not elevated*** - While **ASO titers** are usually elevated following a **streptococcal pharyngitis**, they are often **not elevated** or only mildly elevated in cases of **skin infections** (pyoderma) preceding **post-streptococcal glomerulonephritis (PSGN)**. - The streptococcal products that trigger ASO antibody production are less accessible to the immune system during skin infections compared to pharyngeal infections. *Initially elevated, rapidly fall in 3-4 days* - This pattern of ASO titer change is not typical for a **streptococcal infection** or its sequelae like **PSGN**. - ASO titers usually rise over days to weeks and then decline gradually over months. *Elevated* - **Elevated ASO titers** are common after **streptococcal pharyngitis**, but less consistently after **streptococcal skin infections** (pyoderma), which are indicated by the 4-week history of skin lesions in this case. - The presence of **cola-colored urine**, **edema**, and **hypertension** 4 weeks after skin lesions strongly points to **PSGN** [1] preceded by skin infection. *Increased progressively over 2 weeks* - While ASO titers do rise after infection, a progressive increase over 2 weeks would typically be seen **earlier in the course of the infection**, not 4 weeks after the initial skin lesions. - At 4 weeks post-infection, if elevated, the titers would usually be peaking or beginning to decline slightly, especially given the timeframe for **PSGN development** [1].
Question 676: A 40-year-old man has been diagnosed with autosomal dominant polycystic kidney disease. How should the cysts be present in USG to call it ADPKD?
- A. ≥2 cysts in each kidney bilaterally (Correct Answer)
- B. ≥4 cysts in each kidney bilaterally
- C. ≥1 cyst in each kidney bilaterally
- D. ≥3 cysts in each kidney bilaterally
Explanation: >=2 cysts in each kidney bilaterally - For individuals aged 30-59 years, a diagnosis of **autosomal dominant polycystic kidney disease (ADPKD)** typically requires at least **2 cysts in each kidney** observed on ultrasound. - This diagnostic criterion helps to differentiate ADPKD from simple renal cysts, which are common in the general population [1]. >=4 cysts in each kidney bilaterally - While more cysts are often present in advanced ADPKD, **4 cysts in each kidney** is a criterion for individuals under 30 years or 60 years and above, not typically for the 30-59 age group. - Using this criterion for a 40-year-old might **underdiagnose earlier stages** of ADPKD. >=1 cyst in each kidney bilaterally - Having only **1 cyst in each kidney** is generally considered insufficient for a definitive diagnosis of ADPKD in a 40-year-old. - This presentation could be consistent with **simple renal cysts**, which are common and not indicative of ADPKD [1]. >=3 cysts in each kidney bilaterally - Although indicative of polycystic kidneys, **3 cysts in each kidney** is a higher threshold than necessary for a 40-year-old. - The established criteria for the 30-59 age group is **2 cysts in each kidney**, making this option overly stringent for a diagnosis.
Question 677: Dialysis patients are prone to develop
- A. Zinc toxicity
- B. Iron toxicity
- C. Aluminium toxicity (Correct Answer)
- D. Lead toxicity
Explanation: ***Aluminium toxicity*** - **Aluminium toxicity** is a significant concern in dialysis patients due to impaired renal excretion of aluminium, which can accumulate from dialysate, oral phosphate binders, or contaminated water. - This toxicity can lead to various complications, including **osteomalacia**, **encephalopathy**, and **anemia**. *Zinc toxicity* - **Zinc toxicity** is uncommon in dialysis patients and typically results from excessive supplementation, not a direct complication of dialysis itself. - Excess zinc can interfere with **copper absorption**, potentially leading to copper deficiency. *Iron toxicity* - While iron supplementation is often used in dialysis patients to treat anemia, **iron toxicity** due to overload is usually managed by monitoring iron levels and adjusting dosage. - It is not an inherent predisposition due to dialysis itself, but rather a potential consequence of therapy. *Lead toxicity* - **Lead toxicity** is primarily associated with environmental exposure and is not a specific complication directly linked to the dialysis process or renal failure [1]. - Lead accumulation is not typically worsened by impaired renal function in the same manner as aluminium [1].
Question 678: Microscopic Hematuria is defined as:
- A. >5 RBCs/high power field (Correct Answer)
- B. >10 RBCs/high power field
- C. >20 RBCs/high power field
- D. >15 RBCs/high power field
Explanation: ***>5 RBCs/high power field*** - The presence of more than 5 **red blood cells (RBCs) per high power field (HPF)** in a properly collected and spun urine sample is the established definition of **microscopic hematuria** [1]. - This threshold indicates an abnormal amount of blood in the urine that is not visible to the naked eye, necessitating further investigation. *>10 RBCs/high power field* - While 10 RBCs/HPF would certainly constitute hematuria, it is a higher threshold than the generally accepted definition for **microscopic hematuria**. - Using this higher threshold might lead to missed diagnoses for individuals with clinically significant, but less pronounced, hematuria. *>20 RBCs/high power field* - A count of 20 RBCs/HPF indicates a significant amount of blood, usually prompting immediate investigation, but it exceeds the **standard definition** for simply identifying the presence of **microscopic hematuria**. - This level of hematuria is unambiguous, but the definition is based on a lower threshold to capture milder cases. *>15 RBCs/high power field* - Similarly to the other incorrect options, 15 RBCs/HPF is above the common and widely accepted definition of **microscopic hematuria**. - The standard definition is set to be sensitive enough to detect potential underlying pathology without being overly broad.
Question 679: Autosomal recessive Polycystic kidneys - all are true except -
- A. Defective gene is PKHD1
- B. Both kidneys show innumerable cysts
- C. USG shows salt and pepper appearance (Correct Answer)
- D. Seen in adults
Explanation: ***USG shows salt and pepper appearance*** - The **"salt and pepper" appearance** on imaging is characteristic of **autosomal dominant polycystic kidney disease (ADPKD)** due to multiple renal cysts of varying sizes and associated vascular calcifications, not autosomal recessive polycystic kidney disease (ARPKD). - ARPKD typically presents with **enlarged, hyperechoic kidneys** with loss of corticomedullary differentiation on ultrasound due to numerous small cysts. *Defective gene is PKHD1* - The dysfunctional gene in **autosomal recessive polycystic kidney disease (ARPKD)** is indeed **PKHD1**, located on chromosome 6. - This gene encodes for **fibrocystin/polyductin**, a protein primarily found in renal and biliary epithelial cells, whose mutation leads to cyst formation. *Both kidneys show innumerable cysts* - ARPKD is characterized by **bilateral involvement** with diffuse dilation of the collecting ducts, leading to innumerable small cysts in both kidneys. - These cysts cause significant **renal enlargement** and can lead to severe renal dysfunction. *Seen in adults* - **Autosomal recessive polycystic kidney disease (ARPKD)** typically manifests in **infancy or childhood**, often prenatally or neonatally. - While some milder forms may present later in childhood, it is **not generally seen in adults**; adult-onset polycystic kidney disease is usually autosomal dominant (ADPKD) [1].
Question 680: Acute hyponatremia in an 8-month-old infant may produce all except:
- A. Diarrhea (Correct Answer)
- B. Vascular collapse
- C. Convulsions
- D. Muscle cramps and weakness
Explanation: ***Diarrhea*** - While diarrhea can lead to **dehydration** and subsequent electrolyte imbalances, it is not a direct symptom caused by acute hyponatremia itself. - In fact, severe diarrhea can be a cause of hyponatremia due to excessive loss of sodium and water from the body or by administration of hypotonic fluids to replace losses. *Vascular collapse* - Severe acute hyponatremia can lead to **cerebral edema**, which increases intracranial pressure and can impair brainstem function, leading to **cardiovascular instability** and vascular collapse. - This is a critical and potentially fatal complication due to the rapid shift of fluid into brain cells. *Convulsions* - Rapidly developing hyponatremia can cause significant **brain swelling (cerebral edema)** as water shifts into brain cells osmotiically. - This increase in intracranial pressure and neuronal dysfunction can manifest as **seizures** or convulsions in infants. *Muscle cramps and weakness* - Hyponatremia directly affects muscle cell function due to altered **water and electrolyte balance**. - This can lead to symptoms such as **muscle cramps**, twitching, and generalized weakness.
Practice by Chapter
Acute Kidney Injury
Practice Questions
Chronic Kidney Disease
Practice Questions
Glomerular Diseases
Practice Questions
Tubulointerstitial Diseases
Practice Questions
Nephrotic and Nephritic Syndromes
Practice Questions
Urinary Tract Infections
Practice Questions
Renal Replacement Therapy
Practice Questions
Fluid and Electrolyte Disorders
Practice Questions
Acid-Base Disorders
Practice Questions
Kidney in Systemic Diseases
Practice Questions
Kidney Stones and Obstructive Uropathy
Practice Questions
Hypertension in Kidney Disease
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free