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Diagnosis and Treatment of Acute Renal Failure
- Acute kidney injury – acute renal failure: causes, pathophysiology and symptoms
- Acute kidney injury – acute renal failure: diagnosis and treatment
Diagnosis of Acute Kidney Injury
History
Identify causes and risk factors, including onset and course of urine output, fluid loss, bleeding, signs of sepsis, hypotension, heart failure, cirrhosis, contrast administration, surgery, trauma, rhabdomyolysis, tumor lysis, urinary retention, flank pain, known kidney function, chronic kidney disease, a solitary kidney, and nephrotoxic medications.
Physical Examination
Assess volume status, blood pressure, heart rate, temperature, signs of sepsis, dyspnea, edema, jugular venous pressure, skin turgor, rash, joint symptoms, lymph nodes, bladder distention, prostate, and neurologic signs of voiding dysfunction.
Urine Tests
Assess urine sediment and culture, urine albumin-to-creatinine ratio, and, when indicated, urine electrolytes, protein excretion, urea, creatinine, osmolality, and pH.
Differential diagnosis based on urine sediment
A bland sediment suggests a prerenal, postrenal, or vascular cause. Granular casts and tubular epithelial cells suggest acute tubular injury; red blood cell casts and dysmorphic red blood cells suggest glomerulonephritis or vasculitis; white blood cell casts suggest interstitial nephritis or pyelonephritis; and crystals may indicate crystal nephropathy, tumor lysis syndrome, medications, or intoxication.
Differential diagnosis based on urine analysis
Urinary sodium excretion can help distinguish prerenal from intrinsic renal causes because tubular injury impairs sodium reabsorption. The fractional excretion of sodium (FeNa) relates sodium excretion to creatinine excretion. It requires urine and serum sodium concentrations (UNa and SNa) and urine and serum creatinine concentrations (UKrea and SKrea). A FeNa below 1 % suggests prerenal AKI; a FeNa above 2–3 % suggests intrinsic renal AKI:
FeNa = (UNa × SKrea)/(SNa × UKrea) × 100
Laboratory Tests
- Complete blood count
- Electrolytes (Na, Cl, K, Ca, Mg, P)
- Venous blood gas
- Creatinine, uric acid, and urea
- LDH, CK, lipase, and liver tests
- Glucose, total protein, albumin, and CRP
- Coagulation tests
Ultrasound
Assess kidney size and parenchymal thickness and exclude hydronephrosis. Assess bladder filling and perform an abdominal ultrasound of other organs as indicated. Assess renal perfusion and the resistive index (RI) when clinically indicated.
Noncontrast Abdominal CT
Consider noncontrast abdominal CT to exclude postrenal AKI, particularly if ultrasound findings are inconclusive.
Kidney Biopsy
Kidney biopsy is indicated in acute allograft dysfunction or unexplained AKI with nephritic urine sediment, including microscopic hematuria, dysmorphic red blood cells, red blood cell casts, and significant proteinuria.
Treatment of Acute Kidney Injury
General Measures
- Correct volume depletion or hypotension
- Review medications and discontinue NSAIDs, ACE inhibitors, aminoglycosides, and other nephrotoxic drugs when appropriate
- Monitor fluid balance and body weight
Urinary Drainage
Place an indwelling urinary catheter to monitor urine output or to treat bladder outlet obstruction. In hydronephrosis without urinary retention, elective or urgent upper urinary tract drainage with a double-J ureteral stent or percutaneous nephrostomy is indicated depending on laboratory findings (potassium, urea, and acidosis).
Treatment of Hyperkalemia
In severe hyperkalemia or ECG changes, first stabilize the myocardial cell membrane with intravenous calcium. Then shift potassium into cells with insulin and glucose and an inhaled beta-2 agonist. Use sodium bicarbonate when metabolic acidosis is present. Remove potassium with loop diuretics if urine output is maintained and use enteral potassium binders as adjunctive treatment. Dialysis is indicated for refractory or life-threatening hyperkalemia.
Diuretics
Diuretics are often tried, but controlled studies have not shown that they reduce mortality or the need for dialysis. They may be used to treat volume overload if they increase urine output, for example, furosemide or mannitol.
Dialysis
Indications include severe refractory hyperkalemia, severe metabolic acidosis, fluid overload with pulmonary edema, and uremic symptoms (pericarditis, neurologic symptoms, or bleeding tendency). In critically ill patients without an emergency indication, current evidence does not support routinely starting dialysis early.
Hemodialysis or hemofiltration
See the section on dialysis.
Peritoneal dialysis
Peritoneal dialysis requires placement of a peritoneal catheter and is indicated for treatment of AKI in infants and young children.
Prognosis
Prognosis depends on the cause, KDIGO stage, age, comorbidities, sepsis, multiorgan failure, volume status, and need for kidney replacement therapy. In survivors, kidney function recovers within 2–3 months. Of patients who require dialysis, 20–60 % become independent of kidney replacement therapy. However, 8–21 % of patients who do not require dialysis progress to end-stage kidney disease within 2–3 years.
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References
Alscher M., D.; Erley, C. & Kuhlmann M., K.
Nosokomiales
akutes Nierenversagen
Dtsch Arztebl, 2019, 116,
149-158
Barbar SD, Wald R, Quenot JP. Acute kidney injury: when and how to start renal replacement therapy. Intensive Care Med. 2025 Jun;51(6):1172-1175. doi: 10.1007/s00134-025-07933-x.
KDIGO AKI Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements. 2012;2(1):1–138. https://kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-Guideline-English.pdf
Deutsche Version: Therapie der akuten Niereninsuffizienz
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