Vascular Diseases of the Kidney — MCQs
All are seen in Nephrotic syndrome except
In the context of bilateral renal artery stenosis, which antihypertensive drug is considered contraindicated?
What is the most likely diagnosis in a patient presenting with hypertension, proteinuria, and renal failure?
In shigella dysentery associated hemolytic uremic syndrome, the false statement is ?
Hyperplastic arteriolitis with necrotizing arteriolitis is seen in ?
Most common cause of persistent hypertension in a child with intrinsic renal disease is -
Which of the following is TRUE about Nephrotic Syndrome?
Thrombotic thrombocytopenic purpura is a syndrome characterized by which of the following?
All the following are features of Polycystic disease of kidneys EXCEPT:
IgA nephropathy is not associated with which of the following?
Vascular Diseases of the Kidney Indian Medical PG Practice Questions and MCQs
Question 1: All are seen in Nephrotic syndrome except
- A. Atherosclerosis
- B. Thrombo-embolism
- C. Lipiduria
- D. Increased protein C levels (Correct Answer)
Explanation: ***Increased protein C levels*** - In **nephrotic syndrome**, there is an **increased urinary loss of anticoagulant proteins**, including **Protein C** and **Protein S**, leading to a state of **hypercoagulability**. [1] - Therefore, **Protein C levels are decreased**, not increased, making this the exception. *Atherosclerosis* - **Hyperlipidemia**, a hallmark of nephrotic syndrome, contributes significantly to **accelerated atherosclerosis** due to dysregulation of lipid metabolism. - The increased levels of **LDL cholesterol** and other lipoproteins promote plaque formation and arterial stiffening. *Thrombo-embolism* - Patients with nephrotic syndrome are at a significantly **increased risk of thromboembolic events**, such as deep vein thrombosis and pulmonary embolism, due to a **hypercoagulable state**. - This state results from the **urinary loss of anticoagulant proteins** (e.g., antithrombin III, Protein C, Protein S) and increased levels of procoagulant factors (e.g., fibrinogen, factor V, factor VIII). *Lipiduria* - **Lipiduria**, the presence of lipids in the urine, is a characteristic feature of nephrotic syndrome, often manifested as **oval fat bodies** and **fatty casts**. [1] - This occurs due to the increased glomerular permeability that allows lipoproteins to filter into the urine. [1]
Question 2: In the context of bilateral renal artery stenosis, which antihypertensive drug is considered contraindicated?
- A. Beta-blockers
- B. Calcium channel blockers
- C. ACE inhibitors (Correct Answer)
- D. Diuretics
Explanation: ***ACE inhibitors*** - In bilateral renal artery stenosis, ACE inhibitors can precipitate **acute kidney injury** by severely reducing **glomerular filtration pressure**, as both kidneys rely on **angiotensin II** for maintaining this pressure [1]. - They inhibit the production of **angiotensin II**, leading to **efferent arteriolar dilation** and a drop in glomerular hydrostatic pressure, which is critical for filtration in stenosed kidneys [2]. *Beta-blockers* - Beta-blockers are generally considered safe and effective in treating hypertension associated with renal artery stenosis, as they do not directly interfere with **renal autoregulation** in the same critical way as ACE inhibitors. - They lower blood pressure by reducing **cardiac output** and inhibiting renin release but do not acutely compromise **glomerular filtration** in the presence of stenosis. *Calcium channel blockers* - Calcium channel blockers are safe to use in bilateral renal artery stenosis and are often effective in controlling blood pressure. - They dilate **afferent arterioles**, which can actually help maintain or improve **glomerular filtration rate** by increasing blood flow to the glomerulus. *Diuretics* - Diuretics can be used cautiously in renal artery stenosis to manage blood pressure and fluid overload. - However, aggressive diuresis can lead to intravascular volume depletion, which might exacerbate **renal hypoperfusion** in already stenosed kidneys.
Question 3: What is the most likely diagnosis in a patient presenting with hypertension, proteinuria, and renal failure?
- A. Mycosis fungoides
- B. Wegener's granulomatosis (Correct Answer)
- C. Invasive aspergillosis
- D. Sarcoidosis
Explanation: ***Wegener's granulomatosis*** - This condition, now known as **Granulomatosis with Polyangiitis (GPA)**, classically presents as a triad of **upper respiratory tract disease**, **lower respiratory tract disease**, and **renal disease** [1]. - The renal involvement often manifests as **glomerulonephritis**, leading to **hypertension**, **proteinuria**, and potentially rapid progression to **renal failure** [2]. *Mycosis fungoides* - This is a **cutaneous T-cell lymphoma** primarily affecting the skin, presenting with patches, plaques, and tumors. - It typically does not involve the kidneys in a manner that would cause **hypertension**, **proteinuria**, and **renal failure**. *Invasive aspergillosis* - This is a serious **fungal infection** most commonly seen in **immunocompromised individuals**, affecting the lungs and other organs. - While it can cause systemic illness, it does not typically present with the classic triad of **hypertension**, **proteinuria**, and **renal failure** as a primary finding. *Sarcoidosis* - This is a **multisystem inflammatory disease** characterized by the formation of **non-caseating granulomas** in various organs, most commonly the lungs and lymph nodes. - While renal involvement can occur, it's less common and doesn't typically present with the acute, severe combination of **hypertension**, **proteinuria**, and **renal failure** seen in GPA.
Question 4: In shigella dysentery associated hemolytic uremic syndrome, the false statement is ?
- A. Hepatic failure (Correct Answer)
- B. Leucocytosis
- C. Thrombotic angiopathy
- D. Neurological abnormalities
Explanation: Detailed assessment of the complications of Hemolytic Uremic Syndrome (HUS) following Shigella infection shows that hepatic failure is not a characteristic component. ***Hepatic failure*** - **Hepatic failure** is not a typical hallmark or direct complication of **Shiga toxin-producing E. coli (STEC) HUS**, which primarily targets the kidneys. - The primary organs affected in **HUS** are the **kidneys (acute kidney injury)**, brain (neurological symptoms), and hematopoietic system (thrombocytopenia, microangiopathic hemolytic anemia) [2]. *Leucocytosis* - **Leucocytosis** (elevated white blood cell count) is a common finding in **Shigella dysentery**, reflecting the systemic inflammatory response to the infection. - It can be a predictive marker for the severity of **HUS** development in patients with **STEC** infection. *Thrombotic angiopathy* - **Thrombotic angiopathy** is the underlying pathological process in **HUS**, characterized by **microvascular thrombosis** and **endothelial damage** [1]. - These microthrombi lead to **thrombocytopenia**, **microangiopathic hemolytic anemia**, and **ischemic organ damage**, particularly in the kidneys [1], [2]. *Neurological abnormalities* - **Neurological abnormalities** such as seizures, altered mental status, and strokes can occur in a significant proportion of **HUS** patients. - These complications are due to **cerebral microthrombosis** and **endothelial damage** in the brain, affecting blood flow and neuronal function.
Question 5: Hyperplastic arteriolitis with necrotizing arteriolitis is seen in ?
- A. Buerger's disease
- B. Benign hypertension
- C. Malignant hypertension (Correct Answer)
- D. Diabetes
Explanation: ***Malignant hypertension*** - Characterized by **hyperplastic arteriolitis** and **necrotizing arteriolitis** [1][2], is a severe form of hypertension that typically leads to end-organ damage. - These vascular changes are associated with a markedly elevated blood pressure, often exceeding **180/120 mmHg**, and can result in acute renal failure or **hemorrhagic strokes**. *Benign hypertension* - Generally presents with **minimal vascular changes** and is not associated with the severe arteriolar alterations seen in malignant hypertension. - It does not commonly lead to **acute target organ damage**, distinguishing it from malignant hypertension. *Diabetes* - While diabetes can lead to **microvascular complications** such as **diabetic nephropathy**, it does not specifically cause hyperplastic or necrotizing arteriolitis. - Diabetic vascular changes are typically related to **hyaline arteriosclerosis**, not the severe changes seen in malignant hypertension. *Buerger's disease* - Mainly affects small and medium-sized arteries and veins, typically presenting with **thrombosis** and **vasculitis**, but not hyperplastic or necrotizing arteriolitis. - Primarily associated with **smoking** and does not manifest with the severe renovascular complications like malignant hypertension. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, p. 945. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499.
Question 6: Most common cause of persistent hypertension in a child with intrinsic renal disease is -
- A. CGN (Correct Answer)
- B. Obstructive uropathy
- C. Renal tumor
- D. Chronic Pyelonephritis
Explanation: ***CGN*** - **Chronic glomerulonephritis (CGN)** is a leading cause of persistent hypertension in children with intrinsic renal disease due to widespread glomerular damage leading to **renin-angiotensin-aldosterone system** activation and fluid retention. - The damaged kidneys are unable to filter waste and regulate blood pressure effectively, contributing to sustained hypertension. *Chronic Pyelonephritis* - While chronic pyelonephritis can cause hypertension, it is typically due to **scarring and inflammation** affecting renal function. - However, it is not as common a cause of persistent hypertension as CGN in children with intrinsic renal disease. *Obstructive uropathy* - **Obstructive uropathy** is classified as a **post-renal (obstructive) disorder** rather than intrinsic renal disease, though it can lead to secondary renal parenchymal damage. - It can cause hypertension through renal parenchymal damage and **renin release** due to increased pressure, but it is not a primary intrinsic renal disease. *Renal tumor* - **Renal tumors**, such as Wilms' tumor, can cause hypertension through **compression of renal arteries** or increased renin production. - While a significant cause of hypertension, it is generally less common than CGN as a cause of persistent hypertension in children with *intrinsic renal disease* overall.
Question 7: Which of the following is TRUE about Nephrotic Syndrome?
- A. Is characterized by normal or increased GFR
- B. Presents with minimal or no hematuria
- C. Causes hyperlipidemia (Correct Answer)
- D. Is associated with decreased serum albumin levels
Explanation: ***Causes hyperlipidemia*** - **Hyperlipidemia** is a hallmark of nephrotic syndrome, occurring due to increased hepatic synthesis of lipoproteins in response to **hypoalbuminemia** and decreased catabolism of lipids [1]. - The liver attempts to compensate for oncotic pressure loss by increasing lipoprotein production, leading to elevated **cholesterol** and **triglyceride** levels. *Is characterized by normal or increased GFR* - While GFR can initially be normal, it often **decreases** in nephrotic syndrome as renal damage progresses or due to associated conditions like **acute kidney injury**. - There is no characteristic increase in GFR; instead, sustained massive proteinuria is the defining feature. *Presents with minimal or no hematuria* - This statement is generally true for pure nephrotic syndrome, but it's not the most defining characteristic compared to hyperlipidemia. Nephrotic syndrome is primarily about **proteinuria**, not hematuria [2]. - Conditions with significant hematuria are more typical of **nephritic syndromes**, which have different underlying pathophysiologies [2]. *Is associated with decreased serum albumin levels* - This statement is true, but it describes a **consequence** of the massive proteinuria in nephrotic syndrome, not the primary mechanism of disease [1]. - The defining feature of nephrotic syndrome is **massive proteinuria** (protein loss in urine), which *leads* to **hypoalbuminemia** (low serum albumin levels) [2].
Question 8: Thrombotic thrombocytopenic purpura is a syndrome characterized by which of the following?
- A. Thrombocytopenia, anemia, neurological abnormalities, progressive renal failure and fever (Correct Answer)
- B. Thrombocytopenia, anemia, neurological abnormalities, progressive hepatic failure and fever
- C. Thrombocytopenia, normal anemia, neurological abnormalities, progressive renal failure and fever
- D. Thrombocytopenia, anemia, no neurological abnormalities, progressive renal failure and fever
Explanation: ***Thrombocytopenia, anemia, neurological abnormalities, progressive renal failure and fever*** - Thrombotic thrombocytopenic purpura is characterized by **thrombocytopenia** and **microangiopathic hemolytic anemia**, along with neurological and renal complications [1][2]. - The presence of **fever** and other systemic symptoms is consistent with this **thrombotic microangiopathy** syndrome [1]. *Thrombocytosis, anemia, neurologic abnormalities, progressive renal failure and fever* - This option incorrectly lists **thrombocytosis** rather than **thrombocytopenia**, which is a hallmark of thrombotic thrombocytopenic purpura (TTP) [1]. - While it includes anemia, the absence of thrombocytopenia makes it inconsistent with TTP's classic presentation [2]. *Thrombocytopenia, anemia, neurologic abnormalities, progressive hepatic failure and fever* - Although it correctly states **thrombocytopenia** and **anemia**, it incorrectly identifies **progressive hepatic failure** instead of **renal failure**, which is a key feature of TTP [1]. - The presence of neurological abnormalities and fever does align with TTP; however, the hepatic failure aspect is misleading. *Thrombocytosis, anemia neurologic abnormalities, progressive renal failure and fever* - Again, this option incorrectly notes **thrombocytosis**, contradicting the characteristic finding of **thrombocytopenia** found in TTP [1]. - While other features align with TTP's clinical picture, the thrombocytosis excludes this option from being correct [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 947-948. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668.
Question 9: All the following are features of Polycystic disease of kidneys EXCEPT:
- A. Erythrocytosis (Correct Answer)
- B. Renal failure
- C. Haematuria
- D. Hypertension
Explanation: ***Erythrocytosis*** - While other renal conditions like **renal cell carcinoma** can cause erythrocytosis due to increased **erythropoietin** production, it is generally **not a typical feature** of Polycystic Kidney Disease (PKD). - Patients with PKD usually have **normal or even low erythropoietin levels** despite compromised kidney function, and anemia is more common, particularly as **renal failure progresses**. *Renal failure* - **Progressive cyst growth** leads to replacement of normal kidney parenchyma, inevitably culminating in **end-stage renal disease** [1] in the majority of patients. - This is a hallmark feature, often necessitating **dialysis or transplant** later in life for individuals with autosomal dominant polycystic kidney disease (ADPKD) [2]. *Haematuria* - **Gross or microscopic hematuria** is a common symptom in PKD, often resulting from **cyst rupture** [1], bleeding into a cyst, or the passage of a calculus due to urinary stasis. - It can be a presenting symptom and can cause significant pain and anxiety for patients. *Hypertension* - **Hypertension** is an early and frequent complication of PKD, often preceding any significant decline in glomerular filtration rate. - It is primarily caused by activation of the **renin-angiotensin-aldosterone system (RAAS)** [3] due to arterial compression and ischemia from expanding cysts. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 951-955. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 544-545. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 520-521.
Question 10: IgA nephropathy is not associated with which of the following?
- A. Focal mesangial proliferation
- B. Gross hematuria concurrent with upper respiratory infection
- C. Immunofluorescence deposits contain IgA and IgG
- D. Decreased complement level (Correct Answer)
Explanation: ***Decreased complement level*** - IgA nephropathy is typically associated with **normal serum complement levels** (C3 and C4), which is an important distinguishing feature. - Unlike post-streptococcal glomerulonephritis or lupus nephritis where complement levels are **low/decreased**, IgA nephropathy does not cause systemic complement consumption. - While complement activation does occur locally in the glomerulus (via lectin and alternative pathways), it does not lead to a decrease in serum complement levels. *Focal mesangial proliferation* - This is a **common histological finding** in IgA nephropathy, reflecting the proliferative response to IgA deposition in the mesangium. - The mesangial cells proliferate in an attempt to clear the immune deposits. *Gross hematuria concurrent with upper respiratory infection* - This is a **classic clinical presentation** of IgA nephropathy, often referred to as **synpharyngitic hematuria**. - The episode of gross hematuria typically occurs **within 1-2 days** of the onset of an upper respiratory tract infection, distinguishing it from post-streptococcal glomerulonephritis where hematuria appears 1-3 weeks later. *Immunofluorescence deposits contain IgA and IgG* - The defining feature of IgA nephropathy on immunofluorescence is the **predominant deposition of IgA**, often accompanied by C3. - While IgA is the primary immunoglobulin, **IgG and IgM can also be present** in variable amounts, but IgA must be the dominant or co-dominant immunoglobulin for the diagnosis.
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