Nephrology — MCQs
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A 47-year-old HIV-positive man presents with weakness, HIV nephropathy, and adrenal insufficiency. He is taking trimethoprim-sulfamethoxazole for PCP prophylaxis and triple-agent antiretroviral treatment. He was recently started on spironolactone for ascites due to alcoholic liver disease. Physical examination reveals normal vital signs, but his muscles are diffusely weak. Frequent extrasystoles are noted. He has mild ascites and 1+ peripheral edema. Laboratory studies show a serum creatinine of 2.5 mg/dL with a potassium value of 7.3 mEq/L. ECG shows peaking of the T-waves and QRS widening to 0.14 seconds. Once the patient is stabilized and the T-waves have normalized, it is important to review the potential causes of his hyperkalemia and to take steps to prevent this from happening again. As you consider the pathophysiology of each factor, which of the following statements is true?
A patient being treated for leukemia develops unilateral flank pain. Radiologic studies demonstrate a dilated renal pelvis and dilation of the upper one-third of the corresponding ureter. A stone with which of the following compositions is most likely causing this patient's problems?
All of the following are true regarding Bartter syndrome except?
All of the following are true about Bartter syndrome except?
A 57-year-old male is admitted to the hospital for a suspected kidney infection (likely pyelonephritis). The patient is placed on intravenous antibiotic therapy but continues to have a temperature of 103°F after 3 days of therapy. The urine culture grows lactose-fermenting Gram-negative bacilli which are pan drug-sensitive. On examination, he appears ill and has marked left flank tenderness. Ultrasound depicts a specific finding. What is the most likely diagnosis?
A 24-year-old man has a urine analysis that is positive for blood. The microscopic examination of the urine is negative for casts or red blood cells. Which of the following is the most likely diagnosis?
What is the most common cause of renal papillary necrosis?
Normal anion gap metabolic acidosis can occur in which of the following conditions?
Which of the following statements about kidney injury molecule-1 (KIM-1) is false?
Which of the following is seen in nephrotic syndrome?
Nephrology Indian Medical PG Practice Questions and MCQs
Question 321: A 47-year-old HIV-positive man presents with weakness, HIV nephropathy, and adrenal insufficiency. He is taking trimethoprim-sulfamethoxazole for PCP prophylaxis and triple-agent antiretroviral treatment. He was recently started on spironolactone for ascites due to alcoholic liver disease. Physical examination reveals normal vital signs, but his muscles are diffusely weak. Frequent extrasystoles are noted. He has mild ascites and 1+ peripheral edema. Laboratory studies show a serum creatinine of 2.5 mg/dL with a potassium value of 7.3 mEq/L. ECG shows peaking of the T-waves and QRS widening to 0.14 seconds. Once the patient is stabilized and the T-waves have normalized, it is important to review the potential causes of his hyperkalemia and to take steps to prevent this from happening again. As you consider the pathophysiology of each factor, which of the following statements is true?
- A. Trimethoprim-sulfamethoxazole, used for Pneumocystis infection prophylaxis, causes hypokalemia and therefore would have prevented this patient's presentation.
- B. Spironolactone, a diuretic for ascites in cirrhosis, acts as a competitive aldosterone inhibitor at the collecting duct, decreasing potassium excretion and causing hyperkalemia. (Correct Answer)
- C. The patient likely had pseudo-hyperkalemia due to hemolysis caused by using a small needle and rough specimen handling, leading to potassium release into the serum.
- D. Once hospitalized, the patient may receive heparin for DVT prophylaxis, which would help ameliorate hyperkalemia in the ensuing days.
Explanation: ### Educational Explanation **1. Why Option B is Correct:** This patient presents with severe, symptomatic hyperkalemia (K+ 7.3 mEq/L) with ECG changes (peaked T-waves, QRS widening) [1]. **Spironolactone** is a potassium-sparing diuretic that acts as a competitive antagonist of the mineralocorticoid receptor in the cortical collecting duct [2]. By blocking aldosterone, it inhibits the reabsorption of sodium and the secretion of potassium and hydrogen ions [2]. In the setting of **chronic kidney disease (CKD)** (Creatinine 2.5 mg/dL), the risk of life-threatening hyperkalemia is significantly amplified. **2. Analysis of Incorrect Options:** * **Option A:** Trimethoprim (in TMP-SMX) actually **causes hyperkalemia**, not hypokalemia. It structurally resembles amiloride and blocks the epithelial sodium channels (ENaC) in the distal nephron, reducing the electrical gradient for potassium secretion. * **Option C:** While hemolysis can cause pseudohyperkalemia, this patient has **clinical symptoms** (muscle weakness) and **ECG changes** (QRS widening), confirming true, life-threatening hyperkalemia [1]. * **Option D:** Heparin (including LMWH) **worsens hyperkalemia**. It inhibits adrenal synthesis of aldosterone by reducing the number and affinity of angiotensin II receptors in the zona glomerulosa. **3. Clinical Pearls for NEET-PG:** * **Drug-Induced Hyperkalemia:** Always look for "The Deadly Trio" in questions: ACE inhibitors/ARBs, Spironolactone, and NSAIDs/TMP-SMX. * **HIV & Hyperkalemia:** HIV patients are at high risk due to **HIV-associated nephropathy (HIVAN)**, adrenal insufficiency (Addison’s), and medications like TMP-SMX and Pentamidine. * **ECG Progression:** Peaked T waves → PR prolongation/P wave flattening → QRS widening → Sine wave pattern → Ventricular Fibrillation [3]. * **Management Priority:** The first step in hyperkalemia with ECG changes is **Calcium Gluconate** (membrane stabilization), followed by insulin/glucose (shift) and finally removal (hemodialysis or resins) [1].
Question 322: A patient being treated for leukemia develops unilateral flank pain. Radiologic studies demonstrate a dilated renal pelvis and dilation of the upper one-third of the corresponding ureter. A stone with which of the following compositions is most likely causing this patient's problems?
- A. Calcium salts
- B. Cholesterol
- C. Cystine
- D. Uric acid (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Uric acid** **1. Why Uric Acid is Correct:** The clinical scenario describes a patient with **leukemia** presenting with obstructive uropathy (flank pain and hydroureteronephrosis). In hematologic malignancies like leukemia, there is a high rate of cell turnover. When these patients undergo chemotherapy, it can trigger **Tumor Lysis Syndrome (TLS)**. The rapid breakdown of nucleic acids leads to the overproduction of purine metabolites, resulting in **Hyperuricemia**. Production is specifically increased in leukemia because of the increased breakdown of uric-acid-rich white blood cells [1]. Uric acid is poorly soluble in the acidic environment of the distal tubule and collecting ducts. This leads to the precipitation of **Uric Acid crystals**, forming stones that cause acute urinary tract obstruction [2]. On imaging, these stones are typically **radiolucent** (not visible on plain X-ray) but can be seen on CT or via secondary signs like hydronephrosis on ultrasound. **2. Why Incorrect Options are Wrong:** * **A. Calcium salts:** Calcium oxalate is the most common type of kidney stone overall [3]. However, it is not specifically associated with leukemia or rapid cell turnover. * **B. Cholesterol:** Cholesterol is a component of gallstones, not renal calculi. * **C. Cystine:** Cystine stones are rare and caused by an autosomal recessive defect in the transport of dibasic amino acids (COLA: Cystine, Ornithine, Lysine, Arginine). They typically present in childhood or young adulthood. **3. NEET-PG High-Yield Pearls:** * **Morphology:** Uric acid crystals are characteristically **rhomboid** or rosette-shaped and are **pleomorphic**. * **Radiology:** Uric acid stones are **Radiolucent** on X-ray but **Radiopaque** on Non-Contrast CT (NCCT). * **Management:** Prevention involves aggressive hydration, **allopurinol** (xanthine oxidase inhibitor), or **rasburicase** (urate oxidase), and **alkalization of urine** (pH > 6.5) using potassium citrate [2]. * **Risk Factor:** Acidic urine is the single most important factor for uric acid stone formation.
Question 323: All of the following are true regarding Bartter syndrome except?
- A. Hypokalemic alkalosis
- B. Hypomagnesuria (Correct Answer)
- C. Congenital sensorineural hearing defect
- D. Associated with Barttin mutation
Explanation: Bartter syndrome is a group of autosomal recessive disorders characterized by a defect in the thick ascending limb (TAL) of the loop of Henle, mimicking the effect of loop diuretics (Furosemide). **Why Option B is the Correct Answer (The False Statement):** In Bartter syndrome, there is typically **Hypermagnesuria** (increased magnesium in urine), not hypomagnesuria. The defect in the TAL disrupts the positive transepithelial potential difference normally required for the paracellular reabsorption of magnesium and calcium. This leads to increased urinary excretion of magnesium, which can result in **hypomagnesemia** (low serum magnesium). **Analysis of Incorrect Options:** * **Option A (Hypokalemic alkalosis):** This is a hallmark of Bartter syndrome. Failure of NaCl reabsorption in the TAL leads to increased distal delivery of sodium, which stimulates the Renin-Angiotensin-Aldosterone System (RAAS), causing potassium and hydrogen ion secretion in the collecting duct [1]. * **Option C & D (Hearing defect & Barttin mutation):** **Type IV Bartter syndrome** (Neonatal Bartter with sensorineural deafness) is caused by a mutation in the **BSND gene**, which encodes **Barttin**, a subunit of the ClC-Ka and ClC-Kb chloride channels. These channels are essential for both renal salt reabsorption and the maintenance of endolymph in the inner ear. **NEET-PG Clinical Pearls:** * **Bartter vs. Gitelman:** Bartter syndrome presents early (infancy/childhood) with **hypercalciuria** (loop diuretic-like), whereas Gitelman syndrome presents later (adolescence) with **hypocalciuria** (thiazide-like). * **Key Feature:** Patients often present with polyhydramnios in utero and severe salt wasting postnatally. * **Mnemonic:** **B**artter acts like a **B**ig loop (Loop diuretics), **G**itelman acts like a **G**entle thiazide.
Question 324: All of the following are true about Bartter syndrome except?
- A. Urinary calcium is increased.
- B. Hypokalemic alkalosis is present.
- C. Mineralocorticoid antagonists can be used. (Correct Answer)
- D. Blood pressure is normal.
Explanation: Bartter syndrome is a group of autosomal recessive disorders caused by mutations in the transporters of the **thick ascending limb (TAL)** of the Loop of Henle (e.g., NKCC2, ROMK). It mimics the effect of chronic **Loop diuretic** (Furosemide) use. **1. Why Option C is the correct answer (False statement):** While Bartter syndrome involves secondary hyperaldosteronism, **Mineralocorticoid antagonists (like Spironolactone) are not the primary treatment.** The mainstay of management is **NSAIDs** (like Indomethacin) because prostaglandins are significantly elevated in Bartter syndrome and drive many of the clinical features. While potassium-sparing diuretics can be used as adjuncts, NSAIDs are the classic pharmacological hallmark for boards. **2. Analysis of other options:** * **Option A (Urinary calcium is increased):** True. Since the TAL is responsible for the reabsorption of calcium (driven by the positive luminal potential), a defect here leads to **hypercalciuria**. This distinguishes Bartter from Gitelman syndrome (which has hypocalciuria). * **Option B (Hypokalemic alkalosis):** True. Failure of salt reabsorption in the TAL leads to increased sodium delivery to the distal tubule, causing salt wasting, renin-angiotensin-aldosterone system (RAAS) activation, and subsequent K+ and H+ secretion [1]. * **Option D (Blood pressure is normal):** True. Despite high renin and aldosterone levels, patients are typically **normotensive or hypotensive** due to profound renal salt wasting and systemic vasodilation from high prostaglandins. **High-Yield Clinical Pearls for NEET-PG:** * **Bartter vs. Gitelman:** Bartter = "Loop Diuretic" effect (Hypercalciuria); Gitelman = "Thiazide" effect (Hypocalciuria + Hypomagnesemia). * **Presentation:** Bartter often presents in infancy/childhood with polyuria, polydipsia, and growth retardation. * **Key Lab Findings:** Hypokalemia, Metabolic Alkalosis, Hypercalciuria, and High Prostaglandin E2.
Question 325: A 57-year-old male is admitted to the hospital for a suspected kidney infection (likely pyelonephritis). The patient is placed on intravenous antibiotic therapy but continues to have a temperature of 103°F after 3 days of therapy. The urine culture grows lactose-fermenting Gram-negative bacilli which are pan drug-sensitive. On examination, he appears ill and has marked left flank tenderness. Ultrasound depicts a specific finding. What is the most likely diagnosis?
- A. Hydronephrosis
- B. Nephrolithiasis
- C. Emphysematous pyelonephritis
- D. Perinephric abscess (Correct Answer)
Explanation: ***Perinephric abscess*** - **Persistent high fever** despite 3 days of appropriate antibiotic therapy in pyelonephritis strongly suggests **abscess formation**, as antibiotics cannot penetrate well into enclosed collections. - Ultrasound would show a **hypoechoic fluid collection** in the **perinephric space** surrounding the kidney, which is the key diagnostic finding. *Hydronephrosis* - Would present with **obstructive symptoms** and **dilated renal pelvis** on ultrasound, not persistent fever after antibiotic treatment. - Usually associated with **decreased urine output** and **relief of pain** with positioning, unlike this case. *Nephrolithiasis* - Typically presents with **colicky pain** that radiates to the groin, not constant flank tenderness. - Ultrasound would show **echogenic stones** with **acoustic shadowing**, and fever would resolve with antibiotics if infection was present. *Emphysematous pyelonephritis* - Occurs primarily in **diabetic patients** and involves **gas-forming bacteria** creating emphysema in renal parenchyma. - Ultrasound would show **hyperechoic foci** with **dirty shadowing** from gas, and the organism is typically **Klebsiella** or **E. coli**, not just any lactose-fermenter.
Question 326: A 24-year-old man has a urine analysis that is positive for blood. The microscopic examination of the urine is negative for casts or red blood cells. Which of the following is the most likely diagnosis?
- A. Hematuria
- B. Nephritic syndrome
- C. Renal cell carcinoma
- D. Myoglobinuria (Correct Answer)
Explanation: ### Explanation The core of this question lies in understanding the **discrepancy between the urine dipstick and microscopic examination**. [1] **1. Why Myoglobinuria is Correct:** The standard urine dipstick uses the **pseudoperoxidase activity of hemoglobin** to detect blood. This test cannot distinguish between intact red blood cells (RBCs), free hemoglobin, or **myoglobin**. [1] * In **Myoglobinuria** (often due to rhabdomyolysis), the dipstick will show a "positive for blood" result because myoglobin reacts with the reagent. [1] * However, because there are no actual red cells involved, the **microscopic examination** will show an absence of RBCs and casts. [1], [2] This "positive dipstick, negative microscopy" pattern is a classic diagnostic hallmark for either myoglobinuria or hemoglobinuria. [1] **2. Why the Other Options are Incorrect:** * **A. Hematuria:** By definition, hematuria requires the presence of RBCs in the urine (usually >3 RBCs/HPF). If this were the diagnosis, the microscopic exam would not be negative. [1] * **B. Nephritic Syndrome:** This is characterized by the "nephritic sediment," which includes hematuria, **dysmorphic RBCs, and RBC casts**. The negative microscopy rules this out. [1] * **C. Renal Cell Carcinoma:** This typically presents with gross or microscopic hematuria. Again, intact RBCs would be visible under the microscope. **3. NEET-PG High-Yield Pearls:** * **The "Dipstick-Microscopy Gap":** If Dipstick is (+) for blood but Microscopy is (-) for RBCs, think: **Myoglobinuria** (check Serum CK) or **Hemoglobinuria** (check for hemolysis/low haptoglobin). [1] * **Rhabdomyolysis:** Common triggers include trauma (crush injury), extreme exertion, statins, or seizures. * **Color Clue:** In myoglobinuria, the urine often appears "cola-colored" or "tea-colored." * **Complication:** The most serious complication of myoglobinuria is **Acute Tubular Necrosis (ATN)** due to the direct toxic effect of myoglobin on renal tubules.
Question 327: What is the most common cause of renal papillary necrosis?
- A. Analgesic nephropathy
- B. Sickle cell disease
- C. Diabetes mellitus (Correct Answer)
- D. Chronic pyelonephritis
Explanation: **Explanation:** Renal Papillary Necrosis (RPN) is an ischemic infarct of the renal papillae, which are particularly vulnerable due to their relatively low blood supply and high osmolality. **Why Diabetes Mellitus is the Correct Answer:** While multiple conditions cause RPN, **Diabetes Mellitus** is statistically the **most common cause** (associated with over 50% of cases). The pathogenesis involves a combination of diabetic microangiopathy (ischemia) and a predisposition to recurrent urinary tract infections (pyelonephritis), which synergistically lead to papillary infarction. **Analysis of Incorrect Options:** * **Analgesic Nephropathy:** Historically a major cause due to phenacetin use, it is now less common. It occurs because NSAIDs inhibit prostaglandins, leading to medullary vasoconstriction and ischemia. * **Sickle Cell Disease/Trait:** A common cause in younger populations. Sickling of RBCs in the hypertonic, hypoxic environment of the renal medulla leads to micro-thrombosis and infarction. * **Chronic Pyelonephritis:** While severe infection can cause RPN, it is usually a secondary factor or occurs in the presence of obstruction or diabetes. **NEET-PG High-Yield Pearls:** * **Mnemonic for Causes (POSTCARDS):** **P**yelonephritis, **O**bstruction, **S**ickle cell, **T**uberculosis, **C**irrhosis, **A**nalgesics, **R**enal vein thrombosis, **D**iabetes mellitus, **S**ystemic vasculitis. * **Clinical Presentation:** Gross hematuria, flank pain (mimicking renal colic due to sloughed papillae obstructing the ureter), and "ring sign" on IVP (contrast surrounding a sloughed papilla). * **Key Distinction:** In Diabetes, RPN is often bilateral; in Sickle Cell, it can occur even in asymptomatic carriers (Sickle Cell Trait).
Question 328: Normal anion gap metabolic acidosis can occur in which of the following conditions?
- A. Renal failure (Correct Answer)
- B. Liver failure
- C. Severe anemia
- D. Malignancy
Explanation: **Explanation:** Metabolic acidosis is categorized based on the **Anion Gap (AG)**, calculated as $[Na^+] - ([Cl^-] + [HCO_3^-])$. **1. Why Renal Failure is Correct:** Renal failure is a unique cause that can present with both types of acidosis depending on the stage: * **Early Renal Failure (CKD Stages 1-4):** Often presents as **Normal Anion Gap Metabolic Acidosis (NAGMA)**. This occurs because the kidneys lose the ability to excrete ammonium ($NH_4^+$) and reabsorb bicarbonate, but the glomerular filtration rate (GFR) is still high enough to filter titratable acids (phosphates/sulfates). * **Advanced Renal Failure (ESRD/Stage 5):** As GFR drops significantly (<15-20 mL/min), the kidney can no longer filter unmeasured anions like phosphates, sulfates, and organic acids. These accumulate, leading to a **High Anion Gap Metabolic Acidosis (HAGMA)**. **2. Why Incorrect Options are Wrong:** * **Liver Failure, Severe Anemia, and Malignancy:** These conditions are classically associated with **Type A or Type B Lactic Acidosis** [1]. Lactic acid dissociates into lactate (an unmeasured anion), which increases the anion gap, resulting in **HAGMA**, not NAGMA. **3. NEET-PG High-Yield Pearls:** * **NAGMA Mnemonic (USED CARP):** **U**reterosigmoidostomy, **S**aline (Normal Saline infusion), **E**ndocrine (Addison’s), **D**iarrhea (most common cause), **C**arbonic anhydrase inhibitors (Acetazolamide), **A**mmonium chloride, **R**enal tubular acidosis (RTA), **P**ancreatic fistula [1]. * **HAGMA Mnemonic (MUDPILES):** **M**ethanol, **U**remia (Advanced Renal Failure), **D**KA, **P**ropylene glycol, **I**soniazid/Iron, **L**actic acidosis, **E**thylene glycol, **S**alicylates [1]. * **Key Distinction:** In NAGMA, the drop in $HCO_3^-$ is compensated by a rise in $Cl^-$, which is why it is also called **Hyperchloremic Metabolic Acidosis** [1].
Question 329: Which of the following statements about kidney injury molecule-1 (KIM-1) is false?
- A. KIM-1 is a novel biomarker of acute kidney injury (AKI).
- B. KIM-1 is abundantly expressed in distal tubular cells. (Correct Answer)
- C. KIM-1 can be detected shortly after ischemic injury in the urine.
- D. All the above statements are false.
Explanation: Kidney Injury Molecule-1 (KIM-1) is a type I transmembrane glycoprotein that has emerged as a highly specific and sensitive **biomarker for proximal tubular injury**. **1. Why Option B is the correct (False) statement:** KIM-1 is **not** expressed in distal tubular cells. In a healthy kidney, KIM-1 is virtually undetectable. However, following an ischemic or nephrotoxic insult, it is **markedly upregulated specifically in the proximal tubular epithelial cells**. It plays a role in tubular regeneration and acts as a phosphatidylserine receptor, transforming epithelial cells into "semi-professional" phagocytes to clear apoptotic debris. **2. Analysis of other options:** * **Option A:** KIM-1 is indeed a **novel biomarker** of AKI [1]. Unlike Serum Creatinine, which is a marker of function and rises late, KIM-1 is a marker of structural damage. * **Option C:** KIM-1 is highly stable and its ectodomain is shed into the lumen, allowing it to be **detected in the urine shortly after injury** (within hours), long before a rise in creatinine occurs. **High-Yield Clinical Pearls for NEET-PG:** * **Localization:** Proximal Tubule (High-yield: Contrast this with **NGAL**, which is expressed in both proximal and distal tubules). * **FDA Status:** KIM-1 is one of the few biomarkers qualified by the FDA for use in drug development to monitor nephrotoxicity. * **Predictive Value:** Higher urinary KIM-1 levels are associated with an increased risk of progressing to Chronic Kidney Disease (CKD). * **Other AKI Biomarkers:** NGAL (earliest), IL-18, L-FABP, and IGFBP-7 × TIMP-2 (Cell cycle arrest markers).
Question 330: Which of the following is seen in nephrotic syndrome?
- A. Proteinuria less than 3.5 gm/day
- B. Hyperalbuminemia
- C. Hypercoagulability (Correct Answer)
- D. Hypertension
Explanation: **Explanation:** Nephrotic syndrome is characterized by a triad of massive proteinuria, hypoalbuminemia, and generalized edema [1]. The correct answer is **Hypercoagulability**, which is a significant complication of this condition [1]. **1. Why Hypercoagulability is correct:** The loss of plasma proteins through the damaged glomerular basement membrane [2] includes natural anticoagulants, most notably **Antithrombin III (AT-III)**, Protein C, and Protein S. Simultaneously, the liver increases the synthesis of pro-coagulant factors (like Fibrinogen) and there is increased platelet aggregation. This imbalance shifts the hemostatic system toward a pro-thrombotic state, increasing the risk of deep vein thrombosis (DVT) and **Renal Vein Thrombosis (RVT)**, especially in Membranous Nephropathy [1]. **2. Why other options are incorrect:** * **A. Proteinuria less than 3.5 gm/day:** By definition, nephrotic-range proteinuria must be **>3.5 gm/24 hours** (in adults). Values below this are considered sub-nephrotic or characteristic of nephritic syndrome [2]. * **B. Hyperalbuminemia:** Nephrotic syndrome causes **Hypoalbuminemia** (<3 g/dL) due to massive urinary loss and catabolism of albumin in the proximal tubule [1]. * **C. Hypertension:** While hypertension can occur in some types of nephrotic syndrome (like FSGS), it is a classic hallmark of **Nephritic Syndrome** [2]. Nephrotic syndrome is primarily defined by metabolic and protein disturbances rather than inflammatory hematuria and hypertension. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of RVT:** Membranous Nephropathy. * **Hyperlipidemia:** Seen in nephrotic syndrome due to compensatory hepatic synthesis of lipoproteins (LDL/VLDL) in response to low oncotic pressure [1]. * **Infection Risk:** Patients are prone to infections (e.g., *S. pneumoniae*) due to the loss of **Immunoglobulins (IgG)** and Complement factors in urine.
Practice by Chapter
Acute Kidney Injury
Practice Questions
Chronic Kidney Disease
Practice Questions
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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