Nephrology

A

• Acute Kidney Injury — Diagnosis and Management

  Acute kidney injury is an abrupt decline in kidney function recognized by a rise in serum creatinine, reduced urine output, or both. Evaluation should identify prerenal hypoperfusion, intrinsic renal injury, and postrenal obstruction while immediately correcting reversible threats such as shock, nephrotoxins, hyperkalemia, severe acidosis, and urinary obstruction. Management is cause-directed and includes careful fluid assessment, medication adjustment, electrolyte surveillance, and timely nephrology consul
• Acute Kidney Injury — Evaluation & Management

  Acute kidney injury is an abrupt decline in kidney function identified by a rise in serum creatinine, reduced urine output, or both. Evaluation should determine the timing, likely mechanism, reversibility, volume status, medication exposures, and presence of urgent complications. Management is cause directed and emphasizes hemodynamic optimization, nephrotoxin stewardship, electrolyte control, and kidney replacement therapy only when clinically indicated.
• Acute Kidney Injury — KDIGO Staging, Volume Optimization, and RRT Indications

  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.
• Acute Symptomatic Hyponatremia — 3% Saline Bolus, Desmopressin Clamp, and Relowering Safety

  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.
• Acute Symptomatic Hyponatremia — Rapid Correction Protocol

  Severe symptomatic hyponatremia requires hypertonic saline boluses and tight correction limits to avoid osmotic demyelination; use DDAVP clamp strategies to prevent overcorrection.
• Alport Syndrome — Hereditary Nephritis, Hearing Loss & Genetic Diagnosis

  Alport syndrome is a COL4A3/COL4A4/COL4A5-related disorder of type IV collagen that causes persistent glomerular hematuria, progressive proteinuric kidney disease, sensorineural hearing loss, and characteristic ocular findings. Diagnosis increasingly relies on molecular genetic testing, and early renin-angiotensin system blockade can delay kidney failure.
• Anemia of CKD — Iron, ESA, and HIF‑PH Inhibitors

  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.

C

• Calciphylaxis in ESRD — Painful Necrotic Lesions and Multimodal Therapy

  Dialysis patient with exquisitely painful violaceous plaques progressing to necrosis—consider calcific uremic arteriolopathy (calciphylaxis).

H

• Hemodialysis — Vascular Access Issues & Infection Prevention

  AV fistula preferred over graft over catheter; meticulous infection prevention and prompt management of access complications are critical.
• Hyperkalemia — ECG Risks & Treatment Algorithm

  Immediate threat when ECG changes or K+ ≥6.0. Stabilize membrane, shift K+ intracellularly, and remove K+; address causes and prevent recurrence.
• Hypermagnesemia — Toxicity and Treatment

  Hypermagnesemia is usually caused by magnesium administration or impaired renal excretion and can progress from nausea and loss of deep tendon reflexes to hypotension, bradycardia, respiratory paralysis, heart block, and cardiac arrest. Stop magnesium exposure, stabilize airway and circulation, give IV calcium for serious toxicity, enhance renal elimination when feasible, and use dialysis for severe toxicity with renal failure.
• Hypernatremia — Diagnosis and Management

  Hypernatremia is a deficit of water relative to body sodium, usually from unreplaced free-water loss and less often from sodium gain. Neurologic injury reflects both the hypertonicity itself and, in chronic disease, the risk of overly rapid reversal after cerebral adaptation. Management therefore requires restoration of circulation first when needed, then calculated but repeatedly reassessed replacement of free water and treatment of the cause.
• Hypernatremia — Free Water Correction

  Hypernatremia reflects a deficit of water relative to sodium and is usually caused by impaired access to water, excessive renal water loss, or gastrointestinal loss. Restore circulation first if shock is present, then replace the free-water deficit gradually while identifying ongoing losses and avoiding overly rapid correction of chronic hypernatremia.
• Hypokalemia — Diagnosis & Potassium Repletion

  Evaluate urinary K+ loss and acid–base status to identify renal vs extrarenal causes; replete potassium and correct magnesium; monitor for arrhythmias.
• Hyponatremia — Diagnosis & Management

  Hyponatremia is a water-balance disorder defined by low serum sodium and should be classified by measured serum osmolality, symptoms, chronicity, and volume physiology. Severe neurologic symptoms require prompt hypertonic saline, while all patients require protection from overly rapid correction and treatment of the underlying cause.

I

• IgA Nephropathy — Diagnosis & Treatment

  Risk‑stratify by proteinuria, eGFR, and MEST‑C pathology; maximize supportive care (RAASi, SGLT2i); consider immunosuppression in high‑risk cases.

L

• Life-Threatening Hyperkalemia — Stabilize, Shift, and Remove Potassium

  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.
• Life‑Threatening Hyperkalemia — Membrane Stabilization, K+ Shift, and Removal

  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.
• Lithium Toxicity — Fluids and Dialysis

  Lithium toxicity produces gastrointestinal symptoms, tremor, ataxia, confusion, dysarthria, myoclonus, seizures, and coma, with severity influenced by acute versus chronic exposure and renal function. Stop lithium, restore intravascular volume with isotonic saline, follow serial lithium concentrations, and use hemodialysis for severe poisoning according to clinical and EXTRIP criteria.

M

• Membranous Nephropathy — Risk Stratification & Treatment

  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.
• Minimal Change Disease (Adult) — Diagnosis & Steroid Therapy

  Adult MCD presents with nephrotic syndrome; high corticosteroid responsiveness; evaluate for secondary causes; manage complications of nephrosis.

P

• Peritoneal Dialysis — Modality Selection & Complications

  Peritoneal dialysis modality selection considers lifestyle and residual renal function; prevent and treat peritonitis; manage catheter and exit‑site care meticulously.

R

• Rhabdomyolysis — Diagnosis and Management

  Rhabdomyolysis is skeletal-muscle breakdown with release of CK, myoglobin, potassium, phosphate, and other intracellular contents. Diagnose with a compatible clinical context and substantial CK elevation, identify dangerous hyperkalemia and compartment syndrome early, provide goal-directed isotonic crystalloid to preserve renal perfusion, and avoid routine bicarbonate, mannitol, or dialysis solely to prevent AKI.
• Rhabdomyolysis — Fluids and Complication Prevention

  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.

S

• Secondary Hyperparathyroidism in CKD — Management

  Manage with phosphate control, vitamin D repletion/analogs, and calcimimetic therapy; avoid hypercalcemia and oversuppression; align with dialysis protocols.
• Severe Hyperkalemia — ECG Changes, Membrane Stabilization, and Dialysis Triggers

  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.
• Severe Hypokalemia — Urgent Repletion

  Severe hypokalemia can cause muscle weakness, ileus, rhabdomyolysis, atrial and ventricular arrhythmias, and respiratory failure. Urgent management requires ECG monitoring, identification and correction of magnesium deficiency, potassium replacement by the safest effective route, treatment of the cause, and frequent reassessment to avoid rebound hyperkalemia.
• Severe Symptomatic Hyponatremia — Hypertonic Saline

  Severe symptomatic hyponatremia is a neurologic emergency caused by hypotonic cerebral edema. Treat seizures, coma, severe confusion, or other major neurologic manifestations promptly with bolus 3% saline, aim for a small early sodium rise sufficient to reverse symptoms, and then slow correction to prevent osmotic demyelination.