Nephrology Practice Questions

Q: A young adult presents with hematuria following a sore throat. Diagnosis?

IgA nephropathy. ***IgA nephropathy*** - **IgA nephropathy** often presents with **recurrent hematuria** that occurs concurrently with or shortly after an **upper respiratory tract infection** (like a sore throat) [1]. - This condition is characterized by the deposition of **IgA immune complexes** in the glomeruli, leading to microscopic or macroscopic hematuria [1], [3]. *Henoch-Schönlein purpura (HSP)* - While HSP is also an **IgA vasculitis** that can cause hematuria, it typically presents with a classic tetrad of symptoms: **palpable purpura**, **arthralgia**, **abdominal pain**, and **renal involvement**. - The patient in this case only presents with hematuria following a sore throat, lacking the other characteristic features of HSP. *Post-streptococcal glomerulonephritis (PSGN)* - **PSGN** typically presents with hematuria, edema, and hypertension about **1-3 weeks after** a streptococcal infection (e.g., strep throat) [2]. - The key differentiator is the **latency period** between the infection and the onset of renal symptoms, which is usually shorter or absent in IgA nephropathy [1]. *Goodpasture syndrome (GPS)* - **Goodpasture syndrome** is an autoimmune disease characterized by antibodies against the **glomerular basement membrane (GBM)**, leading to rapidly progressive glomerulonephritis and often pulmonary hemorrhage [3]. - It does not typically present with hematuria immediately following a sore throat and is not directly linked to such antecedent infections in the same manner as IgA nephropathy or PSGN.

Q: Which of the following is not a complication of nephrotic syndrome?

Hypoalbuminemia. ***Hypoalbuminemia*** - **Hypoalbuminemia** is a *defining feature* of nephrotic syndrome, not a complication. - It results from the **massive urinary protein loss** that is central to the diagnosis of nephrotic syndrome [1]. *Infection risk* - Patients with nephrotic syndrome are at increased risk of **infections** due to urinary loss of immunoglobulins and complement factors [1]. - This often manifests as **peritonitis**, cellulitis, or pneumonia. *Hypertension* - **Hypertension** is a common complication, often due to **fluid retention**, activation of the **renin-angiotensin-aldosterone system**, and underlying renal dysfunction [1]. - It contributes to the progression of kidney disease and cardiovascular morbidity. *Hypercoagulability* - **Hypercoagulability** is a significant complication caused by urinary loss of **antithrombin III** and other anticoagulant proteins, coupled with increased synthesis of prothrombotic factors [1]. - This increases the risk of **thromboembolic events**, such as deep vein thrombosis and pulmonary embolism.

Q: Which of the following is not a complication of hypokalemia?

Cerebral edema. ***Cerebral edema*** - **Cerebral edema** is typically associated with **hyponatremia** (low sodium levels), which causes hypotonicity in the extracellular fluid leading to water shifting into brain cells. - Hypokalemia primarily impacts neuromuscular and cardiac function and does not directly cause brain swelling due to fluid shifts. *Quadriparesis* - **Severe hypokalemia** can lead to **muscle weakness**, which can progress to flaccid paralysis affecting all four limbs (quadriparesis). - This occurs due to alterations in the **resting membrane potential** of muscle cells, making them less excitable. *Ventricular Tachycardia* - Hypokalemia can cause **cardiac arrhythmias**, including **ventricular tachycardia** and **fibrillation**, by prolonging repolarization and increasing myocardial excitability. - It can also lead to characteristic electrocardiogram (ECG) changes such as **flattened T waves**, **ST segment depression**, and prominent **U waves**. *Diabetes insipidus* - **Nephrogenic diabetes insipidus** can be a complication of chronic hypokalemia, where the kidneys become resistant to the effects of **antidiuretic hormone (ADH)**. - This results in the inability to concentrate urine, leading to **polyuria** (excessive urination) and **polydipsia** (excessive thirst).

Q: A patient presents with metabolic acidosis and increased anion gap. Which is most consistent with this presentation?

Lactic acidosis. ***Lactic acidosis*** - **Lactic acidosis** is a common cause of **high anion gap metabolic acidosis**, resulting from increased lactate production or decreased lactate clearance [1]. - Conditions like **sepsis**, **shock**, and severe hypoxia can lead to increased anaerobic metabolism and subsequent lactic acid accumulation [1]. *Renal tubular acidosis* - This condition is characterized by **metabolic acidosis** but typically presents with a **normal anion gap** (non-anion gap metabolic acidosis) [1]. - It involves impaired acid excretion or bicarbonate reabsorption by the renal tubules, not an accumulation of unmeasured anions [1]. *Hyperaldosteronism* - **Hyperaldosteronism** typically causes **hypokalemia** and **metabolic alkalosis**, not metabolic acidosis [2]. - Excess aldosterone leads to increased sodium reabsorption and potassium/hydrogen ion excretion [2]. *Diarrhea* - Severe **diarrhea** leads to a loss of bicarbonate from the gastrointestinal tract, causing a **normal anion gap metabolic acidosis** [1]. - It does not involve the accumulation of unmeasured acids that would increase the anion gap.

Q: Which condition is characterized by hemoptysis, glomerulonephritis, and the presence of anti-glomerular basement membrane antibodies?

Goodpasture syndrome. ***Goodpasture syndrome*** - This condition is precisely defined by the triad of **hemoptysis** (due to pulmonary hemorrhage), rapidly progressive **glomerulonephritis**, and the presence of **anti-glomerular basement membrane (GBM) antibodies** [2], [4]. - The anti-GBM antibodies target collagen type IV in the basement membranes of the glomeruli and alveoli, leading to simultaneous lung and kidney damage [3], [4]. *Granulomatosis with polyangiitis (Wegener's granulomatosis)* - While it can cause **hemoptysis** and **glomerulonephritis**, it is primarily associated with **ANCA (anti-neutrophil cytoplasmic antibodies)**, specifically c-ANCA, not anti-GBM antibodies [2]. - It also commonly involves **upper and lower respiratory tract granulomatous inflammation**, which is not a defining feature in the prompt [4]. *Systemic lupus erythematosus (SLE)* - SLE can cause **glomerulonephritis** (lupus nephritis) and, less commonly, pulmonary hypertension and hemorrhage, but it is not typically associated with prominent **hemoptysis** as a primary presenting symptom in this context [1], [2]. - SLE is characterized by a wide range of autoimmune phenomena and the presence of **antinuclear antibodies (ANA)**, not anti-GBM antibodies. *Sarcoidosis* - Sarcoidosis is a multisystem **granulomatous disease** that most commonly affects the lungs (causing cough and dyspnea) and lymph nodes. - It sporadically causes **glomerulonephritis** but is not associated with **hemoptysis** or the presence of **anti-GBM antibodies**.

Q: A 40-year-old woman presents with facial swelling, periorbital edema, and proteinuria. Which condition is most likely responsible for her symptoms?

Nephrotic syndrome. ***Nephrotic syndrome*** - The combination of **facial swelling**, **periorbital edema**, and **proteinuria** is the classic triad of symptoms defining nephrotic syndrome [1]. - This syndrome is characterized by **massive proteinuria** (>3.5g/day), leading to **hypoalbuminemia**, which in turn causes reduced plasma oncotic pressure and fluid extravasation into interstitial spaces [1]. *Congestive heart failure* - While it can cause **edema**, it typically presents with **dependent edema** (e.g., in legs), **dyspnea**, and signs of fluid overload, not prominent facial or periorbital edema as a primary symptom with proteinuria. - **Proteinuria** can occur in chronic heart failure due to reduced renal perfusion, but it is usually not the massive proteinuria characteristic of nephrotic syndrome. *Liver cirrhosis* - Can cause **peripheral edema** and **ascites** due to portal hypertension and hypoalbuminemia, but **facial and periorbital edema** are less common as primary presenting symptoms. - While some **proteinuria** can be seen in chronic liver disease, it's typically milder and not the massive proteinuria seen in nephrotic syndrome. *Hypothyroidism* - Can cause **non-pitting edema** (myxedema), often described as puffy facial features and periorbital swelling, due to the accumulation of **hyaluronic acid** in the interstitial space. - However, **significant proteinuria** is not a characteristic feature of hypothyroidism; hence, it's less likely to explain the full constellation of symptoms.

Q: Which of the following factors most directly contributes to the development of edema in patients with nephrotic syndrome?

Hypoalbuminemia. Hypoalbuminemia - Nephrotic syndrome is defined by significant proteinuria leading to a decrease in serum albumin levels [2]. - Albumin is the primary protein responsible for maintaining oncotic pressure within the capillaries, and its deficiency (<3 g/dL) leads to fluid shifts from the intravascular space to the interstitial space, causing edema [1], [2]. Increased capillary permeability - While increased capillary permeability can cause edema, it is not the primary mechanism in nephrotic syndrome. - In nephrotic syndrome, the problem is loss of protein from the capillaries, rather than the capillaries themselves becoming excessively leaky to fluid in general. Hypertension - Hypertension can exacerbate edema by raising hydrostatic pressure, but it is not the initial or primary cause of edema in nephrotic syndrome [1]. - Edema in nephrotic syndrome can occur even in normotensive patients due to severe hypoalbuminemia [2]. Hypernatremia - Hypernatremia indicates high sodium levels in the blood, which would typically cause water to shift into the intravascular space, thus drawing fluid out of the interstitial space. - In actuality, patients with nephrotic syndrome often experience some degree of sodium retention, which contributes to fluid overload, but it is not the most direct cause of fluid moving from the capillaries into the interstitial tissue [3].

Q: A 58-year-old woman with chronic kidney disease has a serum potassium level of 5.8 mEq/L. What is the most likely cause?

Decreased renal excretion. ***Decreased renal excretion*** - **Chronic kidney disease (CKD)** is the most common cause of **hyperkalemia** due to the kidneys' reduced ability to excrete potassium [3]. - In CKD, the glomerular filtration rate (GFR) is significantly low, impairing the normal homeostatic mechanisms for potassium balance [3]. *Increased dietary potassium intake* - While excessive dietary potassium can contribute to hyperkalemia, it is usually not the sole cause in an individual with normal kidney function due to efficient renal excretion [1]. - In the context of CKD, even a moderate increase in dietary potassium can be problematic, but the primary underlying issue remains the impaired excretion. *Increased aldosterone secretion* - **Aldosterone** promotes potassium excretion in the kidneys; therefore, increased aldosterone secretion would typically lead to **hypokalemia**, not hyperkalemia [1]. - Conditions causing increased aldosterone (e.g., primary hyperaldosteronism) are known to cause potassium wasting [4]. *Hypercalcemia* - **Hypercalcemia** refers to elevated calcium levels in the blood and does not directly cause hyperkalemia. - Although it can cause cardiovascular and renal complications, it does not typically lead to a direct increase in potassium levels [2].

Q: What is the most effective treatment for reducing the progression of diabetic nephropathy?

Blood pressure control with ACE inhibitors. ***Blood pressure control with ACE inhibitors*** - **Angiotensin-converting enzyme (ACE) inhibitors** are crucial as they reduce intraglomerular pressure and proteinuria, thereby slowing the progression of **diabetic nephropathy** [1]. - Their nephroprotective effects go beyond blood pressure reduction, specifically targeting the **renin-angiotensin-aldosterone system (RAAS)** which is implicated in renal damage in diabetes [1]. *Optimal glycemic control* - While essential for overall diabetes management and preventing microvascular complications, **glycemic control** alone does not have as significant an impact on the progression of established diabetic nephropathy as RAAS blockade [1], [4]. - Its primary role is in **preventing the initial onset** and early stages of diabetic nephropathy rather than significantly reducing its progression once macroalbuminuria is present [2]. *High protein intake* - **High protein intake** can worsen diabetic nephropathy by increasing the glomerular filtration burden and contributing to hyperfiltration and kidney damage. - In patients with established diabetic nephropathy, a **low-protein diet** is often recommended to reduce renal workload and potentially slow disease progression. *Diuretic therapy* - **Diuretics** are used to manage volume overload and hypertension in patients with kidney disease but do not directly reduce the progression of diabetic nephropathy [3]. - They primarily alleviate symptoms and lower blood pressure through fluid removal, but they lack the specific **renal protective mechanisms** of ACE inhibitors [3].

Q: What is the most common cause of acute kidney injury in hospitalized patients?

Acute tubular necrosis. ### Acute tubular necrosis - **Acute tubular necrosis (ATN)** is the most frequent cause of acute kidney injury (AKI) in hospitalized patients, often resulting from **ischemia** or **nephrotoxic drugs** [1]. - It involves direct injury to the **renal tubular epithelial cells**, leading to their dysfunction and subsequent decline in kidney function [1]. *Glomerulonephritis* - **Glomerulonephritis** is an inflammatory condition affecting the **glomeruli**, which are the filtering units of the kidney. - While it can cause AKI, it is a less common cause compared to ATN, and its presentation typically involves **hematuria** and **proteinuria** [1]. *Renal artery stenosis* - **Renal artery stenosis** primarily causes chronic kidney disease and **renovascular hypertension** due to reduced blood flow to the kidney. - Although severe, acute occlusion can cause AKI, it is not the most common cause of AKI in the general hospitalized population. *Drug-induced nephropathy* - **Drug-induced nephropathy** encompasses various forms of kidney damage caused by medications, including **acute interstitial nephritis** and direct tubular toxicity. - While a significant contributor to AKI, many cases of drug-induced AKI are specifically forms of ATN or allergic interstitial nephritis, making ATN a broader and more common category [1].

Question 1

A young adult presents with hematuria following a sore throat. Diagnosis?

Accepted Answer

IgA nephropathy

Answer

Henoch-Schönlein purpura (HSP)

Answer

Post-streptococcal glomerulonephritis (PSGN)

Answer

Goodpasture syndrome (GPS)

Question 2

Which of the following is not a complication of nephrotic syndrome?

Accepted Answer

Hypoalbuminemia

Answer

Infection risk

Answer

Hypertension

Answer

Hypercoagulability

Question 3

Which of the following is not a complication of hypokalemia?

Accepted Answer

Cerebral edema

Answer

Quadriparesis

Answer

Ventricular Tachycardia

Answer

Diabetes insipidus

Question 4

A patient presents with metabolic acidosis and increased anion gap. Which is most consistent with this presentation?

Accepted Answer

Lactic acidosis

Answer

Renal tubular acidosis

Answer

Hyperaldosteronism

Answer

Diarrhea

Question 5

Which condition is characterized by hemoptysis, glomerulonephritis, and the presence of anti-glomerular basement membrane antibodies?

Accepted Answer

Goodpasture syndrome

Answer

Granulomatosis with polyangiitis (Wegener's granulomatosis)

Answer

Systemic lupus erythematosus (SLE)

Answer

Sarcoidosis

Question 6

A 40-year-old woman presents with facial swelling, periorbital edema, and proteinuria. Which condition is most likely responsible for her symptoms?

Accepted Answer

Nephrotic syndrome

Answer

Congestive heart failure

Answer

Liver cirrhosis

Answer

Hypothyroidism

Question 7

Which of the following factors most directly contributes to the development of edema in patients with nephrotic syndrome?

Accepted Answer

Hypoalbuminemia

Answer

Increased capillary permeability

Answer

Hypertension

Answer

Hypernatremia

Question 8

A 58-year-old woman with chronic kidney disease has a serum potassium level of 5.8 mEq/L. What is the most likely cause?

Accepted Answer

Decreased renal excretion

Answer

Increased dietary potassium intake

Answer

Increased aldosterone secretion

Answer

Hypercalcemia

Question 9

What is the most effective treatment for reducing the progression of diabetic nephropathy?

Accepted Answer

Blood pressure control with ACE inhibitors

Answer

Diuretic therapy

Answer

Optimal glycemic control

Answer

High protein intake

Question 10

What is the most common cause of acute kidney injury in hospitalized patients?

Accepted Answer

Acute tubular necrosis

Answer

Glomerulonephritis

Answer

Renal artery stenosis

Answer

Drug-induced nephropathy

Nephrology — MCQs

Nephrology — MCQs

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