Nephrology
Showing 27 of 27 topics
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Identify prerenal, intrinsic, or postrenal causes; review nephrotoxins; manage volume status, electrolytes, and acid–base; start dialysis for standard indications.
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Define AKI by KDIGO criteria; assess volume, meds, obstruction; manage with fluids or diuresis as appropriate; avoid nephrotoxins; consider dialysis for AEIOU indications.
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AKI is defined by creatinine rise or oliguria. Apply KDIGO staging, optimize hemodynamics and volume, avoid nephrotoxins, and initiate renal replacement therapy for standard emergent indications or persistent severe AKI after optimization.
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Severe symptoms (seizures, coma) require immediate 3% saline boluses to raise Na+ by 4–6 mEq/L quickly; then maintain controlled correction using a desmopressin clamp and tailored fluids to avoid overcorrection and osmotic demyelination. Aggressively treat the underlying cause.
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Severe symptomatic hyponatremia requires hypertonic saline boluses and tight correction limits to avoid osmotic demyelination; use DDAVP clamp strategies to prevent overcorrection.
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Correct iron deficiency first; use ESAs for persistent anemia with careful Hb targets; consider HIF‑PH inhibitors per labeling; individualize based on symptoms and risk.
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Dialysis patient with exquisitely painful violaceous plaques progressing to necrosis—consider calcific uremic arteriolopathy (calciphylaxis).
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AV fistula preferred over graft over catheter; meticulous infection prevention and prompt management of access complications are critical.
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Immediate threat when ECG changes or K+ ≥6.0. Stabilize membrane, shift K+ intracellularly, and remove K+; address causes and prevent recurrence.
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Hypotension, bradycardia, and hyporeflexia suggest toxicity; stop magnesium sources, give IV calcium for cardiac stabilization, provide fluids and diuretics, and dialyze when needed.
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Differentiate water deficit from sodium gain; correct gradually (generally ≤10–12 mEq/L per 24 h) using hypotonic fluids; address the underlying cause.
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Treat dehydration and hyperosmolality by calculating free water deficit and replacing slowly; correct underlying cause and monitor sodium closely.
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Evaluate urinary K+ loss and acid–base status to identify renal vs extrarenal causes; replete potassium and correct magnesium; monitor for arrhythmias.
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Classify by serum osmolality and volume; check urine osmolality and urine Na; treat severe symptoms with hypertonic saline; limit correction to ≤8–10 mEq/L in 24 h to avoid ODS.
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Risk‑stratify by proteinuria, eGFR, and MEST‑C pathology; maximize supportive care (RAASi, SGLT2i); consider immunosuppression in high‑risk cases.
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Treat hyperkalemia with a three-step sequence: stabilize cardiac membrane (IV calcium), shift K+ intracellularly (insulin/dextrose, β-agonists, bicarbonate if acidotic), and remove K+ (diuretics, potassium binders, or dialysis). Continuous ECG monitoring is essential.
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ECG changes or K+ ≥6.0 mEq/L require immediate IV calcium for membrane stabilization, insulin/dextrose and beta‑agonist for intracellular shift, and measures to remove potassium (loop diuretics, binders, or dialysis). Identify and treat precipitating causes.
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Acute or chronic toxicity presents with GI upset, tremor, ataxia, and confusion; give isotonic fluids to enhance clearance and arrange hemodialysis for standard indications.
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Use anti‑PLA2R/THSD7A antibodies and risk stratification (proteinuria, eGFR) to guide therapy; ACEi/ARB and SGLT2i for all; immunosuppression for high‑risk or progressive disease.
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Adult MCD presents with nephrotic syndrome; high corticosteroid responsiveness; evaluate for secondary causes; manage complications of nephrosis.
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Peritoneal dialysis modality selection considers lifestyle and residual renal function; prevent and treat peritonitis; manage catheter and exit‑site care meticulously.
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Muscle breakdown with elevated CK causing AKI risk; aggressive isotonic fluids, treat hyperkalemia, address cause; consider urine alkalinization selectively.
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Identify muscle injury with elevated CK and myoglobinuria; give early isotonic fluids, monitor electrolytes and urine output, and manage complications such as hyperkalemia and AKI.
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Manage with phosphate control, vitamin D repletion/analogs, and calcimimetic therapy; avoid hypercalcemia and oversuppression; align with dialysis protocols.
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Hyperkalemia with ECG changes or K+ ≥6.5 mEq/L is a medical emergency. Stabilize the myocardium with IV calcium, shift potassium intracellularly with insulin/dextrose (± beta-agonists, bicarbonate if acidosis), and remove potassium via diuretics, binders, or hemodialysis. Identify and correct precipitants.
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Recognize muscle weakness and arrhythmia risk; correct magnesium, give potassium cautiously IV or PO, and monitor ECG and levels.
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Neurologic symptoms from low sodium require prompt 3 percent saline boluses with careful monitoring to avoid overcorrection; consider desmopressin clamp strategy.
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