Hypertensive Nephrosclerosis (Study Outline) 1. Background Definition: Chronic kidney damage resulting from long-standing hypertension leading to progressive nephron loss and CKD. Pathophysiology: Chronic systemic hypertension → hyaline arteriolosclerosis of afferent/efferent arterioles → ischemic injury to nephrons. Leads to glomerulosclerosis, interstitial fibrosis, and tubular atrophy. Types: Benign nephrosclerosis: gradual progression; associated with essential HTN. Malignant nephrosclerosis: due to severe/accelerated HTN → rapid renal failure and microangiopathic changes. Epidemiology: Common cause of CKD; more prevalent in African American patients due to APOL1 gene risk variants. 2. History Long-standing hypertension (often poorly controlled). Typically asymptomatic early; identified through elevated blood pressure and mild kidney dysfunction. Gradual development of symptoms of CKD: fatigue, nocturia, edema (later stages). Malignant hypertension history clues: headaches, vision changes, chest pain, neurologic symptoms. 3. Exam Findings Blood pressure: chronically elevated; may be severe in malignant nephrosclerosis. Signs of CKD progression: peripheral edema, crackles (fluid overload). Malignant HTN signs (if present): Retinal hemorrhages/exudates, papilledema. Neurologic deficits. Cardiovascular findings: LV hypertrophy or displaced PMI may be present due to chronic HTN. 4. Making the Diagnosis Labs: Mild proteinuria (usually

Metabolic Acidosis (Study Outline) 1. Background Definition: A primary decrease in HCO₃⁻ with low blood pH (12 (lab dependent). High AG clues: Lactic acidosis → elevated lactate. Renal failure → ↑ BUN/Cr. DKA → elevated serum ketones, high glucose. Toxins → osmolar gap (ethanol surrogates). Normal AG (hyperchloremic) clues: RTA → urine pH abnormal patterns. Diarrhea → history of GI losses. Carbonic anhydrase inhibitors. Additional tests: Serum osmolality, ketones, lactate, toxicology screening as indicated. Urinalysis for RTA evaluation. Gold Standard: ABG and serum chemistry confirming ↓ pH, ↓ HCO₃⁻, and AG classification. 5. Management (Exam Concepts) General principles: Correct underlying cause conceptually. Monitor electrolytes (especially K⁺). Avoid nephrotoxins; adjust medication dosing. High AG causes (concept-level): DKA: manage hyperglycemia/ketosis principles. Lactic acidosis: address tissue hypoxia/shock source. Uremia: consider renal replacement therapy if severe (AEIOU). Toxins: antidotes or enhanced elimination principles (e.g., dialysis in selected toxins). Normal AG causes: Diarrheal losses: conceptual volume/electrolyte correction. Renal tubular acidosis: manage acid-base imbalance at concept level. Alkali therapy: May be used conceptually in severe acidosis (pH < severe threshold) or RTA. Monitoring: Serial ABGs, electrolytes, renal function. Dialysis indications: refractory acidosis, toxin-associated AG acidosis, recurrent hyperkalemia, or uremic complications. QUESTION A 52‑year‑old man is brought to the emergency department after being found unconscious at home. His wife reports he had been vomiting and having diarrhea for three days. On arrival his vital signs show: heart rate 110/min, respirations 28/min, blood pressure 92/60 mmHg. He appears weak and dehydrated. Laboratory tests show: Arterial blood gas: pH 7.22 (normal 7.35‑7.45), HCO₃⁻ 14 mEq/L (normal 24‑28) Serum electrolytes: Na⁺ 138 mEq/L, Cl⁻ 110 mEq/L, HCO₃⁻ 14 mEq/L BUN/Cr elevated consistent with dehydration What is the most likely acid‑base disorder and its classification? A) High‑anion‑gap metabolic acidosis due to toxin exposureB) Normal anion gap (hyperchloremic) metabolic acidosis due to gastrointestinal bicarbonate lossC) Mixed metabolic acidosis and respiratory acidosis from respiratory failureD) Normal anion gap metabolic alkalosis from vomiting

Rapidly Progressive Glomerulonephritis (RPGN) (Study Outline) 1. Background Definition: A clinical syndrome of glomerular injury characterized by rapid loss of kidney function over days to weeks, often leading to ESRD if untreated. Pathophysiology: Severe glomerular inflammation → crescent formation in Bowman’s space (proliferation of parietal epithelial cells + macrophages). Loss of filtration barrier → hematuria, proteinuria, rapid GFR decline. Major etiologic categories (exam-high yield): Type I: Anti-GBM disease (Goodpasture syndrome) Anti–glomerular basement membrane antibodies; lung involvement common. Type II: Immune Complex–mediated PSGN, IgA nephropathy, lupus nephritis. Type III: Pauci-immune (ANCA-associated vasculitis) Granulomatosis with polyangiitis (c-ANCA), microscopic polyangiitis (p-ANCA), eosinophilic granulomatosis with polyangiitis. 2. History Rapid onset hematuria (tea/cola-colored). Oliguria or anuria—strong warning sign. Systemic symptoms depending on cause: Goodpasture: cough, hemoptysis. ANCA vasculitis: sinusitis, pulmonary symptoms, constitutional complaints. Immune complex diseases: rash (SLE), recent infection (PSGN), arthralgias. Hypertension from fluid retention. Edema (periorbital, peripheral). 3. Exam Findings Vital signs: hypertension common; may see tachypnea if acidosis. Edema: periorbital, dependent. Pulmonary involvement: crackles, hemoptysis (Goodpasture, GPA). Skin findings: purpura (vasculitis), malar rash (SLE). Signs of severe kidney failure: asterixis, uremic symptoms in advanced cases. 4. Making the Diagnosis Urinalysis: Hematuria with RBC casts (nephritic). Proteinuria (usually

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Polycystic Kidney Disease – Autosomal Dominant (ADPKD) (Study Outline) 1. Background Definition: A genetic disorder causing progressive formation and enlargement of numerous kidney cysts → renal enlargement, loss of function, and eventual CKD/ESRD. Genetics: Autosomal dominant inheritance. Mutations in PKD1 (≈85%) or PKD2 (≈15%); PKD1 associated with earlier, more severe disease. Pathophysiology: Cyst formation from renal tubules → expansion → compression of normal parenchyma → ischemia and fibrosis. Epidemiology: Most common life-threatening monogenic kidney disorder. Presents in adulthood (often ages 20–40). Associated extrarenal manifestations: Hepatic cysts (most common). Pancreatic and splenic cysts. Cerebral aneurysms (berry aneurysms). Cardiac valve abnormalities (MVP, AR). Diverticulosis, abdominal wall/inguinal hernias. 2. History Flank or abdominal pain: due to cyst enlargement, bleeding, or infection. Hematuria: microscopic or gross; often from cyst rupture. Hypertension: very common early due to RAAS activation. Recurrent UTIs or pyelonephritis. Nephrolithiasis (uric acid or calcium oxalate). Family history: first-degree relatives frequently affected. Progressive symptoms of CKD later (fatigue, nocturia, edema). 3. Exam Findings Abdominal masses: bilateral, palpable enlarged kidneys (important exam clue). Hypertension (often severe). Signs of CKD: edema, pallor, asterixis (later stages). Liver enlargement if significant hepatic cysts. Neurologic red flags: severe headaches (possible aneurysm). 4. Making the Diagnosis Labs: Proteinuria (usually mild), possible hematuria. Progressive elevation in BUN/Cr with disease advancement. Imaging (high-yield): Ultrasound = first-line test Shows multiple bilateral renal cysts of varying sizes. CT/MRI: used if ultrasound inconclusive. Diagnostic criteria (age-based, classic): ≥3 cysts total (unilateral or bilateral) if age

Post-streptococcal Glomerulonephritis (PSGN) (Study Outline) 1. Background Definition: Immune-mediated nephritic glomerular disease occurring after infection with group A β-hemolytic Streptococcus (pharyngitis or impetigo). Pathophysiology: Immune complex deposition in glomeruli → complement activation (classical pathway) → inflammation → ↓ GFR. Epidemiology: Most common in children (5–12 years), but can occur in adults with more severe disease course. Timing: Pharyngitis: GN develops 1–2 weeks after infection. Impetigo: GN develops 3–6 weeks after infection. Key concept: A post-infectious immune response, not direct bacterial invasion. 2. History Tea- or cola-colored urine (gross hematuria). Recent strep infection: sore throat, fever, impetigo. Oliguria or decreased urine output. Edema: especially periorbital in the morning. Hypertension due to fluid retention. Constitutional symptoms: malaise, mild fever. Adults may report more severe symptoms or signs of volume overload. 3. Exam Findings Vital signs: hypertension is common. Edema: periorbital and peripheral. Signs of fluid overload: crackles, elevated JVP (severe cases). Skin findings: impetigo lesions if recent skin infection. Generally nephritic pattern: less proteinuria than nephrotic syndromes. 4. Making the Diagnosis Urinalysis: Hematuria with RBC casts (key nephritic hallmark). Mild–moderate proteinuria (

Acute Kidney Injury – Postrenal (Study Outline) 1. Background Definition: AKI resulting from obstruction of urine flow anywhere from renal pelvis to urethra, causing ↑ intratubular pressure, ↓ GFR, and potential tubular injury. Pathophysiology: Obstruction → back pressure on nephrons → hydronephrosis → impaired filtration. Prolonged obstruction can lead to intrinsic renal damage. Common causes: Men: BPH (#1), prostate cancer. Stones: ureterolithiasis. Malignancy: pelvic/abdominal tumors compressing ureters. Neurogenic bladder: diabetes, spinal cord injury. Iatrogenic: postoperative urinary retention, anticholinergic meds. Reversibility: Often highest among AKI types if relieved promptly. 2. History Obstructive urinary symptoms: hesitancy, weak stream, dribbling, incomplete emptying. Acute urinary retention: anuria/oliguria with suprapubic discomfort. Flank pain: suggests stones if acute, colicky. Malignancy history: pelvic radiation, abdominal cancers. Medication review: anticholinergics, opioids. Risk factors: BPH, prior stones, pelvic surgery, neurogenic bladder disorders. 3. Exam Findings Bladder distention: suprapubic fullness or tenderness. Prostate enlargement on digital rectal exam (conceptual). Flank tenderness if upper tract obstruction. Hydronephrosis signs may not be evident clinically but appear on imaging. Volume status: often normal; can appear overloaded due to retained urine. 4. Making the Diagnosis Labs: BUN:Cr ratio variable; not a distinguishing feature. May show hyperkalemia, metabolic acidosis if prolonged. Urinalysis: typically nonspecific; may show hematuria (stones) or pyuria (infection). Key evaluation step: Confirm obstruction. Imaging (high-yield): Renal ultrasound = first-line test Shows hydronephrosis, hydroureter. Non-contrast CT useful for stones. Bladder scan: detects urinary retention. Gold Standard: Imaging-confirmed obstruction + improvement after relief of the obstruction. 5. Management (Exam Concepts) Immediate concept-level priorities: Relieve the obstruction promptly to prevent intrinsic damage. Common exam scenarios: Bladder outlet obstruction (BPH): concept: bladder decompression. Stones: support evaluation with imaging; address obstruction as appropriate in exam context. Malignancy/ureteral compression: may require upper tract decompression (concept only). General supportive principles: Monitor electrolytes, especially potassium. Hold nephrotoxic agents. Address post-obstructive diuresis (exam concept: careful monitoring). When to refer/escalate: uncertain diagnosis, bilateral obstruction, recurrent postrenal AKI, complications. QUESTION A 72-year-old man presents to the emergency department with acute-onset lower abdominal discomfort and decreased urine output for the past 24 hours. He reports difficulty initiating urination, a weak stream, and a sensation of incomplete bladder emptying over the last few weeks. His past medical history includes hypertension and benign prostatic hyperplasia. Medications include hydrochlorothiazide and tamsulosin. On examination, his blood pressure is 138/86 mmHg, pulse is 84/min. The bladder is palpable and tender above the pubic symphysis. Renal ultrasound shows bilateral hydronephrosis and a distended bladder.Serum creatinine is 2.8 mg/dL (baseline 1.1 mg/dL). Which of the following is the most appropriate immediate next step in management? A) Administer intravenous isotonic fluidsB) Begin broad-spectrum antibioticsC) Insert a Foley catheterD) Order a non-contrast CT scan of the abdomen and pelvis

End-Stage Renal Disease (ESRD) (Study Outline) 1. Background Definition: The final, irreversible stage of chronic kidney disease in which GFR

Minimal Change Disease (MCD) (Study Outline) 1. Background Definition: A nephrotic syndrome characterized by podocyte foot process effacement on electron microscopy with minimal/no change on light microscopy. Epidemiology: Most common cause of nephrotic syndrome in children. Can also occur in adults (often with more relapsing course). Pathophysiology: T-cell dysfunction → cytokine-mediated podocyte injury → increased glomerular permeability → heavy proteinuria. Associated conditions: Recent infections, allergies/atopy, Hodgkin lymphoma, NSAID exposure (exam clue). Key concept: Despite dramatic proteinuria, renal function often remains normal early. 2. History Sudden onset edema: periorbital (morning), peripheral, or generalized (anasarca). Foamy urine from heavy proteinuria. Recent viral illness—common trigger in children. Potential associations: allergic symptoms, immunologic conditions, or malignancy (e.g., lymphoma). Fatigue, weight gain from fluid retention. 3. Exam Findings Generalized edema: hallmark; can include ascites or pleural effusions. Vital signs: may be normotensive or mildly hypertensive. Signs of hyperlipidemia: rare clinical manifestations such as xanthelasma. Otherwise normal exam: no gross hematuria or systemic inflammatory signs. 4. Making the Diagnosis Urinalysis: Massive proteinuria (>3.5 g/day). Lipiduria; oval fat bodies; fatty casts. Typically no hematuria and no RBC casts. Blood tests: Hypoalbuminemia, hyperlipidemia; normal complement levels. Renal function often normal or mildly impaired. Renal biopsy: Gold Standard in adults or atypical pediatric cases. Light microscopy: essentially normal glomeruli. Electron microscopy: diffuse podocyte foot process effacement (diagnostic hallmark). Diagnosis in children: often clinical, biopsy not always required if presentation is classic. 5. Management (Exam Concepts) General nephrotic syndrome principles: Sodium restriction for edema at the conceptual level. Monitor renal function and electrolytes. Adjust renally cleared medications; avoid nephrotoxins. Immunosuppression concepts: High-yield exam concept: MCD typically responds dramatically to immunosuppressive therapy (no dosing). Edema management: conceptual strategies (e.g., sodium restriction principles). Hyperlipidemia: may require conceptual lipid management in persistent cases. Relapse monitoring: children may have frequent relapses after infections or allergies. Referral: nephrology for confirmation, management of relapses, or atypical features. QUESTION A 5-year-old boy is brought to the pediatrician for swelling around his eyes and legs for the past three days. His mother reports that he recently had a cold about a week ago. He has been more tired than usual and his urine appears frothy. He has no history of rash, joint pain, or recent travel. Vitals show a blood pressure of 100/62 mmHg. Physical exam reveals periorbital and pedal edema. No rash or lymphadenopathy is noted. Laboratory studies: Serum albumin: 1.8 g/dL (3.5–5.0) Total cholesterol: 280 mg/dL Creatinine: 0.4 mg/dL Urinalysis: 4+ protein, no hematuria, oval fat bodies present Complement C3: normal Which of the following best explains the pathophysiology of this patient’s condition? A) Immune complex deposition in the mesangiumB) Immune complex deposition in the subepithelial spaceC) Cytokine-mediated podocyte injuryD) Antibody-mediated damage to the basement membrane

Metabolic Alkalosis (Study Outline) 1. Background Definition: A primary increase in serum HCO₃⁻ leading to elevated blood pH (>7.45), with compensatory hypoventilation (↑ PaCO₂). Pathophysiology: Requires generation of excess bicarbonate and maintenance due to impaired kidney excretion of HCO₃⁻. Frequently associated with volume depletion, RAAS activation, and hypokalemia, which promote HCO₃⁻ retention. Major etiologic categories: Chloride-responsive (volume-depleted): Vomiting, NG suction (loss of gastric acid). Diuretics. Post-hypercapnia correction. Chloride-resistant (volume-expanded): Hyperaldosteronism (primary or secondary). Cushing syndrome. Severe hypokalemia. High-yield concept: Urine chloride helps differentiate causes. 2. History GI losses: nausea, vomiting, recent NG tube suction. Diuretic use: loop/thiazide history. Endocrine symptoms: hypertension, muscle weakness, polyuria (aldosteronism). Neuromuscular symptoms: paresthesias, cramps, tetany (due to associated hypocalcemia). Hypovolemia symptoms: dizziness, thirst, orthostatic lightheadedness. 3. Exam Findings Vitals: may show hypotension (volume depletion) or hypertension (hyperaldosteronism). Signs of hypovolemia: dry mucous membranes, tachycardia, orthostasis. Neurologic: Chvostek/Trousseau signs (alkalosis increases protein-bound Ca²⁺). Cardiac: arrhythmias from hypokalemia. Physical clues to etiology: Abdominal distension/tenderness (vomiting). Cushingoid features (if steroid excess). 4. Making the Diagnosis ABG/BMP: High pH, high HCO₃⁻, compensatory ↑ PaCO₂ (but rarely >60 mm Hg). Serum electrolytes: Low Cl⁻, low K⁺, possibly ↑ aldosterone (if endocrine cause). Urine chloride (high-yield differentiator): 20 mEq/L → Chloride-resistant (hyperaldosteronism, mineralocorticoid excess). Identify precipitating cause: History of vomiting, diuretics, endocrine disease. Gold Standard: ABG + metabolic panel confirming elevated pH and HCO₃⁻, with urine chloride guiding etiology. 5. Management (Exam Concepts) General principles: Correct underlying cause conceptually (GI losses, diuretic effect, endocrine disease). Avoid nephrotoxins; adjust renal dosing. Chloride-responsive alkalosis: Conceptual volume repletion with chloride to allow renal excretion of HCO₃⁻. Address vomiting/NG losses at conceptual level. Chloride-resistant alkalosis: Treat underlying mineralocorticoid excess conceptually. BP control principles. Electrolyte monitoring: Correct hypokalemia and hypochloremia (key for resolving alkalosis). Severe alkalemia: Consider acidifying therapy conceptually in life-threatening cases (exam-level only). Referral: when metabolic alkalosis is severe, recurrent, or linked to endocrine disease. QUESTION A 28-year-old man presents with dizziness, lightheadedness, and persistent nausea. He reports vomiting multiple times daily for the past 4 days due to a viral illness. He denies diarrhea, recent medications, or alcohol use. On examination, he appears dehydrated with dry mucous membranes and orthostatic hypotension. Laboratory results show: Arterial pH: 7.48 HCO₃⁻: 34 mEq/L PaCO₂: 48 mm Hg K⁺: 3.0 mEq/L Cl⁻: 86 mEq/L What is the most appropriate next step in evaluating the cause of his acid-base disorder? A) Measure serum aldosteroneB) Check urine chlorideC) Begin IV saline and potassium chlorideD) Discontinue furosemide therapy