Renal

• Treat the underlying cause — malignancy, pneumonia, CNS disease and drugs (SSRIs, carbamazepine, PPIs) are the usual suspects.
• Fluid restriction is first-line, but often poorly tolerated and slow.
• Oral urea (e.g. 15–30g daily) raises serum sodium through an osmotic diuresis that increases electrolyte-free water excretion.
• Salt tablets combined with low-dose furosemide also increase free water clearance — the loop diuretic blunts urinary concentrating ability, and this works only if renal function is reasonable.

KDIGO stages AKI on two axes — the rise in creatinine and the fall in urine output. Chart both: a patient can meet the criteria on urine output alone while the creatinine still looks reassuring.

Urine with a specific gravity fixed near that of protein-free plasma (about 1.008–1.012) — the kidney can neither concentrate nor dilute. It reflects loss of the concentrating gradient: seen with ageing, chronic kidney disease, sickle cell disease and after tubular injury.

The triad: electrolyte derangement, myoglobinuria, and AKI. A classic diagnostic clue is a urine dipstick strongly positive for blood but with few or no red cells on microscopy — the dipstick reacts to myoglobin, not intact red cells.

• Causes: traumatic (crush injury, prolonged immobility/"found down") and non-traumatic (exertional heat illness, sickle cell disease/trait, impaired sweating, seizures, statins — especially with an interacting drug — stimulants such as cocaine or amphetamines, and other toxins).
• Electrolytes: hyperkalaemia (can be rapid and severe — ECG monitoring), hyperphosphataemia, and early hypocalcaemia from calcium deposition in injured muscle. Correct hyperkalaemia aggressively, but treat hypocalcaemia only if symptomatic or contributing to hyperkalaemia-related cardiac toxicity — calcium released from muscle during recovery can cause rebound hypercalcaemia if you've over-corrected.
• Avoid NSAIDs — they blunt the renal vasodilation the kidney needs to compensate, worsening the AKI.

Investigations: CK trend (typically peaks 24–72 hours after the trigger, then declines once the trigger is removed), renal function and electrolytes, urine microscopy for pigmented casts. Where there's no clear precipitant, consider a myositis/autoimmune panel and an infective screen (e.g. viral myositis).

• Proteinuria >3.5 g/day, hypoalbuminaemia, oedema, hyperlipidaemia — plus hypertension and a markedly increased VTE risk from urinary loss of antithrombin III.
• Common causes: minimal change disease, FSGS, membranous nephropathy, diabetic nephropathy and amyloid.

Work through the acidosis systematically: calculate the anion gap (corrected for albumin), then in a normal-gap acidosis separate renal from gastrointestinal bicarbonate loss — the urinary anion gap is the discriminator.

Loss of chloride-rich, bicarbonate-poor fluid (vomiting, nasogastric losses, aggressive diuresis) contracts the extracellular volume around a fixed quantity of bicarbonate, so serum bicarbonate rises. It is chloride-responsive — the treatment is volume and chloride replacement with normal saline, plus potassium, rather than anything aimed at the pH itself.

• Profound acidosis reduces adrenoceptor responsiveness — catecholamine binding and downstream signalling are impaired, so vascular smooth muscle becomes less responsive to sympathetic drive and vasodilates.
• The result is escalating catecholamine requirements to achieve the same MAP.
• Practical response: add a second agent working through a different receptor — vasopressin acts on V1 receptors, bypassing the adrenoceptor problem.
• Treat the acidosis itself, and consider renal replacement therapy if it is refractory.

• Commonest around puberty and adolescence, but it occurs at any age — including neonates.
• Classic presentation is sudden severe pain with nausea and vomiting, a high-riding testis and absent cremasteric reflex — but a long-standing, infarcted testis may be relatively painless. Pain out of proportion to findings should worry you.
• Salvage rates fall steeply with time — from around 90% within 6 hours to well under 50% beyond 12–24 hours.
• TWIST score components: testicular swelling, hard testis, absent cremasteric reflex, nausea/vomiting, high-riding testis — a high score supports going straight to exploration.
• Ultrasound (whirlpool sign of the twisted spermatic cord) helps when the diagnosis is genuinely uncertain — but manual detorsion can be attempted while waiting.

Leaving a necrotic testis in situ risks the formation of anti-sperm antibodies with potential effects on future fertility — one of the arguments for orchidectomy of a non-viable testis plus contralateral fixation.

Treat symptomatic catheter-associated UTI for 7 days if the response is prompt, extending to 10–14 days for a delayed response or complicated infection. Replace or remove the catheter where possible — biofilm on an old catheter will defeat the antibiotics. Do not treat asymptomatic bacteriuria in a catheterised patient.