Prerenal, intrarenal and postrenal: sorting the cause
Acute kidney injury is classified by where the problem sits relative to the nephron, and that classification determines the correct intervention. Prerenal injury is a perfusion failure: hypovolaemia, haemorrhage, heart failure or shock reduce renal blood flow. The kidney tissue itself is intact, so restoring volume and cardiac output usually restores function if it is done early.
Intrarenal injury is damage to the nephron itself, most commonly acute tubular necrosis caused by prolonged ischaemia or by nephrotoxins such as aminoglycosides, contrast media and non-steroidal anti-inflammatory drugs. Here fluid alone will not fix the problem, and the nursing focus shifts to removing the offending agent, avoiding further nephrotoxic exposure and managing the consequences of lost filtration.
Postrenal injury is an obstruction below the kidney: an enlarged prostate, calculi, tumours or a blocked catheter. The clue in the stem is often a client who suddenly stops producing urine but reports bladder fullness or suprapubic discomfort. Relieving the obstruction — sometimes as simple as checking the catheter for kinks — restores flow.
- •Prerenal: hypotension, dehydration, sepsis, heart failure
- •Intrarenal: nephrotoxic drugs, contrast, prolonged ischaemia, glomerulonephritis
- •Postrenal: BPH, calculi, tumour, obstructed catheter
- •Always check the catheter before assuming the kidney has failed
Phases of acute kidney injury and what to monitor
The oliguric phase brings urine output below four hundred millilitres per day, rising blood urea nitrogen and creatinine, hyperkalaemia, metabolic acidosis and fluid overload. Nursing priorities are strict intake and output measurement, daily weights, fluid restriction, potassium restriction and continuous vigilance for cardiac dysrhythmias.
The diuretic phase is deceptively dangerous. Urine output can rise to several litres a day as tubules begin to recover but cannot yet concentrate urine. Clients lose sodium, potassium and volume rapidly and can become hypovolaemic and hypokalaemic. The nurse who assumes recovery and relaxes monitoring during this phase misses the deterioration the exam is testing.
The recovery phase may take months and glomerular filtration slowly improves. Teaching in this phase focuses on avoiding nephrotoxic medications, maintaining hydration, controlling blood pressure and diabetes, and attending follow-up laboratory monitoring.
| Value | Normal range | Why it matters |
|---|---|---|
| Creatinine | 0.6–1.2 mg/dL | Most specific marker of glomerular filtration |
| BUN | 10–20 mg/dL | Rises with dehydration, GI bleeding and high protein intake |
| Potassium | 3.5–5.0 mEq/L | Above 5.0 risks peaked T waves and fatal dysrhythmias |
| Phosphate | 3.0–4.5 mg/dL | Rises in CKD and drives calcium down |
| Calcium | 9.0–10.5 mg/dL | Falls in CKD; watch for tetany and Chvostek's sign |
| Bicarbonate | 22–26 mEq/L | Falls with metabolic acidosis of renal failure |
Dialysis nursing and access protection
Haemodialysis removes fluid and solutes rapidly, so the classic complications are hypotension, muscle cramps and disequilibrium syndrome, which presents with headache, nausea, restlessness and, in severe cases, seizures caused by rapid urea shifts. Weigh the client before and after treatment, hold antihypertensives when prescribed to do so, and monitor for bleeding because clients receive heparin during the session.
Arteriovenous fistula care is one of the most reliably tested items in the entire renal chapter. Palpate for a thrill and auscultate for a bruit each shift; their absence suggests clotting and requires immediate reporting. Never use that extremity for blood pressure measurement, venipuncture or intravenous insertion, and teach the client to avoid tight clothing, jewellery and sleeping on that arm.
Peritoneal dialysis carries a different risk profile. Cloudy outflow is the hallmark of peritonitis and must be reported promptly. Warm the dialysate before instilling it, use strict aseptic technique with the catheter, and if outflow is sluggish, reposition the client, check for kinks and ensure the bag is below the abdomen before assuming catheter failure.
- •Bruit heard, thrill felt — assess both every shift
- •No blood pressure, venipuncture or IV in the fistula arm
- •Cloudy peritoneal outflow means peritonitis, report immediately
- •Weigh before and after haemodialysis to quantify fluid removal
Hyperkalaemia: the emergency inside renal items
Because the kidney is the main route of potassium excretion, renal failure and hyperkalaemia travel together, and hyperkalaemia is what actually kills these clients. The exam signals it with muscle weakness, paraesthesia, gastrointestinal hyperactivity and, most importantly, electrocardiographic change: tall peaked T waves, a widened QRS complex and eventually a sine wave pattern.
Treatment sequence follows physiology. Calcium gluconate stabilises the myocardium without lowering potassium. Insulin with dextrose, beta agonists and sodium bicarbonate shift potassium into cells temporarily. Only potassium binders and dialysis actually remove potassium from the body. If an item asks for the immediate action in a client with peaked T waves, protecting the heart comes first.
Dietary teaching supports the medical management. Clients should limit bananas, oranges, potatoes, tomatoes, spinach, avocado and salt substitutes, which are often potassium chloride and catch clients who believe they are making a healthy choice.