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The kidneys generate approximately 180 litres of glomerular filtrate each day, with filtration governed by opposing hydrostatic and oncotic pressures. Net filtration pressure equals capillary hydrostatic pressure minus Bowman's capsule pressure minus plasma oncotic pressure, a margin of only about 10 mmHg. When a ureteric stone obstructs flow, pelvic pressure is transmitted back to Bowman's capsule and filtration falls at once, a direct consequence of pressure rather than a reflex. Afferent dilatation or efferent constriction raises capillary pressure and filtration, whereas a rise in plasma protein lowers it. Ultrafiltration belongs to the glomerulus alone; the tubule reabsorbs and secretes.

The proximal tubule reclaims glucose, amino acids, bicarbonate and most filtered sodium and water. Glucose enters through apical SGLT2 and leaves through basolateral GLUT2, and nowhere else along the nephron. The basolateral sodium-potassium pump supplies the gradient for every secondary active transporter. The thick ascending limb carries NKCC2, the furosemide target, and dilutes urine because it is impermeable to water. The distal tubule carries NCC, the thiazide target, while collecting duct principal cells carry ENaC under aldosterone and aquaporin-2 under antidiuretic hormone.

Concentration depends on a hypertonic medulla built by sodium chloride transport in the thick ascending limb and urea recycling in the inner medullary collecting duct. A prolonged low-protein diet therefore lowers hepatic urea, weakens the medullary gradient and reduces concentrating ability. Antidiuretic hormone acts on V2 receptors, raising cyclic AMP and protein kinase A, which move aquaporin-2 vesicles onto the apical membrane. Water then follows the gradient passively, whereas aquaporin-1 sits permanently in the proximal tubule and descending limb.

In chronic kidney disease the endocrine role fails first. As filtration falls, phosphate is retained; hyperphosphataemia, not hypophosphataemia, is the rule. Renal 1-alpha-hydroxylase declines, calcitriol falls and gut calcium absorption drops, while phosphate binds calcium and lowers it further. High phosphate, low calcium, low calcitriol and an early rise in FGF-23 together drive secondary hyperparathyroidism. Sustained parathyroid hormone excess accelerates bone resorption and produces osteitis fibrosa cystica, with lytic brown tumours and subperiosteal resorption. Oversuppression produces adynamic bone instead, so KDIGO 2017 keeps parathyroid hormone between two and nine times the assay's upper limit in dialysis patients. Phosphate is lowered towards the normal range, calcium-based binders are restricted, and calcimimetics, calcitriol or vitamin D analogues restrain the glands. When severe hyperparathyroidism resists medical therapy, parathyroidectomy follows, with vigilance for hungry bone syndrome.

Hypospadias repair preserves the urethral plate and foreskin and corrects chordee, with at least six months between staged operations. In a duplex kidney the Weigert-Meyer rule places the upper-pole ureter inferomedially, prone to ureterocele, and the lower-pole ureter superolaterally, prone to reflux. Storage is sympathetic, through beta-3 receptors that relax the detrusor and alpha-1 receptors that close the bladder neck. Voiding is parasympathetic through M3 receptors, which drive contraction although M2 receptors are more numerous. In a child with a neurogenic bladder, storage pressure of 40 cmH2O or more injures the upper tract. Catheterisation and antimuscarinics therefore aim for low pressure, large capacity and complete emptying.

All filtration is a pressure balance: obstruction raises capsular pressure, and the filtration rate falls at once.
Is phosphate high in renal failure? Yes, and low calcitriol with low calcium then drives parathyroid hormone upwards.
On dialysis, KDIGO keeps parathyroid hormone between two and nine times the upper limit and restricts calcium-based binders.
Lumen-side glucose is reclaimed only in the proximal tubule, powered by the basolateral sodium-potassium pump.

The adrenal cortex is organised into functionally distinct zones: the outer glomerulosa produces aldosterone, the fasciculata produces cortisol and the reticularis produces androgens; catecholamines originate in the separate medulla. Cortisol and androgens answer to ACTH, whereas aldosterone answers to the renin-angiotensin system and to potassium. Secondary adrenal insufficiency from pituitary failure spares aldosterone, and hyperkalaemia with hyponatraemia points to destruction of the gland itself.

Cushing's syndrome is diagnosed in three steps: confirm excess, measure ACTH, then localise. Because cortisol is circadian, a random level proves nothing; screening must bypass the rhythm. An overnight 1 mg dexamethasone test should suppress morning cortisol below 50 nmol/L; 24-hour urinary free cortisol integrates the day, and late-night salivary cortisol captures a lost nadir. A suppressed ACTH indicates an adrenal source or exogenous steroid; a normal or high ACTH indicates a pituitary adenoma or ectopic secretion, classically small cell lung cancer. High-dose dexamethasone suppresses pituitary tumours but not ectopic sources. The cushingoid patient whose ACTH, cortisol and urinary cortisol are all low is taking a synthetic glucocorticoid that the assay cannot see.

Primary aldosteronism is the most common endocrine cause of secondary hypertension, affecting at least 5 per cent of hypertensives. Autonomous aldosterone acts on ENaC in collecting duct principal cells, retaining sodium while potassium and hydrogen are lost. Hypokalaemia, metabolic alkalosis and volume expansion follow, and the expanded volume suppresses renin. Aldosterone escape within one to two weeks prevents oedema, yet hypertension and hypokalaemia persist. Screening uses the aldosterone-to-renin ratio, drawn in the morning after two hours upright, with potassium corrected first, since hypokalaemia suppresses aldosterone. Mineralocorticoid antagonists are withheld for four weeks and ACE inhibitors, angiotensin blockers, dihydropyridines and beta-blockers for two, with verapamil, hydralazine or an alpha-blocker as cover. A saline infusion of 2 litres over four hours confirms the diagnosis when aldosterone remains above 277 pmol/L. Adrenal vein sampling then separates a unilateral adenoma, cured by laparoscopic adrenalectomy, from bilateral hyperplasia, controlled by spironolactone; in renovascular disease, by contrast, renin is high.

Congenital adrenal hyperplasia is a single causal chain. A blocked enzyme lowers cortisol, feedback is lost, ACTH rises and drives hyperplasia, and stranded precursors are diverted towards androgens. Only 21- and 11-hydroxylase deficiencies virilise, and only 11- and 17-hydroxylase deficiencies raise blood pressure. 21-hydroxylase deficiency accounts for over 90 per cent, with raised 17-hydroxyprogesterone, virilised female infants, salt-wasting crisis in the first weeks and low blood pressure. 11-beta-hydroxylase deficiency retains salt through deoxycorticosterone, whereas 17-alpha-hydroxylase deficiency adds absent sexual development.

Chronic glucocorticoids suppress the axis and shrink the adrenals, so abrupt withdrawal precipitates crisis. They also lower calcium by reducing gut absorption and increasing renal loss, so parathyroid hormone rises and bone thins. Adrenal crisis is treated before it is proven: intravenous hydrocortisone and rapid saline, with cortisol and ACTH drawn but never awaited. Phaeochromocytoma is confirmed by plasma or urinary metanephrines, the stable metabolites of an episodic, short-lived secretion. Alpha-blockade with phenoxybenzamine and volume expansion precede any beta-blocker, since unopposed alpha constriction provokes hypertensive crisis.

All screening for cortisol excess bypasses the circadian rhythm: 1 mg dexamethasone overnight, 24-hour urine or late-night saliva, never a random level.
Is renin suppressed while aldosterone is high? Then the adrenal, not the kidney, is driving the hypertension and the hypokalaemia.
On phaeochromocytoma, alpha-blockade and volume expansion come first; a beta-blocker given first invites a hypertensive crisis.
Luminal sodium channels in the collecting duct obey aldosterone, retaining sodium while potassium and hydrogen are lost.

Benign prostatic obstruction reflects both a structural component, arising from glandular enlargement, and a dynamic component, determined by smooth-muscle tone. The static arm runs from testosterone through 5-alpha-reductase to dihydrotestosterone, which drives glandular growth. Finasteride and dutasteride block the enzyme, but the gland shrinks slowly, so benefit takes three to six months and is significant only above about 40 mL. These drugs halve the PSA, so the measured value is doubled when cancer is being followed. The dynamic arm depends on alpha-1A receptors, about 70 per cent of prostatic alpha-1 receptors; tamsulosin and silodosin block them within days at any gland size. Alpha-1D receptors, in the detrusor and spinal cord, are not tamsulosin's main target. Creatinine and renal ultrasound are the least urgent initial tests unless obstruction is suspected.

PSA is organ-specific, not cancer-specific. Prostatitis, infection, digital examination, cycling, ejaculation and benign enlargement all raise it. A raised PSA with pyuria of 50 to 60 leucocytes per high-power field is inflammation until proven otherwise: treat, then repeat the PSA before any biopsy. A raised PSA with a free-to-total ratio below 15 per cent and a hypoechoic lesion points to cancer and warrants MRI-guided or transrectal biopsy. PSA is insensitive for nodal spread, below 40 per cent, so staging relies on pelvic CT or MRI and a bone scan for osteoblastic metastases. Post-prostatectomy erectile dysfunction follows injury to the parasympathetic cavernous nerves in the posterolateral neurovascular bundle.

Renal cell carcinoma is usually clear cell, linked to VHL on chromosome 3p and to smoking. It is the internist's tumour: erythropoietin causes polycythaemia, PTHrP hypercalcaemia and renin hypertension. Stauffer syndrome is hepatic dysfunction without hepatic metastases, driven by interleukin-6 and reversible after nephrectomy. VEGF tyrosine kinase inhibitors treat advanced disease; their commonest adverse effect is hypertension, not hypothyroidism. Angiomyolipoma declares itself by fat density on CT; it is benign, associated with tuberous sclerosis, and treated only above 4 cm. A filling defect in the renal pelvis or ureter suggests urothelial carcinoma, linked to smoking, phenacetin and aristolochic acid. Bladder cancer is urothelial, not adenocarcinoma; smoking is the dominant risk, Schistosoma haematobium drives squamous carcinoma, and painless haematuria is the presentation.

Testicular germ cell tumours divide into seminoma and non-seminoma. Seminoma is radiosensitive and never raises AFP. Non-seminomatous tumours raise AFP through yolk sac or embryonal elements and are treated with orchidectomy and BEP chemotherapy. Bleomycin scars the lung, and cisplatin injures the kidney and cochlea. Cryptorchidism raises cancer risk, and orchidopexy does not lower it; it only makes the testis examinable.

Erection begins with nitric oxide, which raises cyclic GMP and relaxes cavernosal smooth muscle. PDE5 degrades cyclic GMP, so sildenafil sustains the erection; slight inhibition of retinal PDE6 explains transient blue vision. Nitrates also raise cyclic GMP, so their combination causes profound hypotension and is an absolute contraindication. Rifampicin induces CYP3A4 and merely weakens the drug; it is not a contraindication. Myocardial infarction within six months, severe hypotension and aortic stenosis remain serious cautions.

All alpha-blockers relax prostatic smooth muscle through alpha-1A receptors within days, whatever the gland size.
Is the PSA raised with pus cells in the urine? Treat the infection first and repeat the test before any biopsy.
On imaging, fat density inside a renal mass means angiomyolipoma, benign until it grows beyond 4 cm.
Luminal narrowing by a gland above 40 mL responds to a 5-alpha-reductase inhibitor, which halves the PSA within six months.

Urinary stone formation is favoured when dissolved constituents become supersaturated, allowing crystals to form and grow according to the local balance of promoters and inhibitors. Calcium, oxalate, urate, cystine, struvite and matrix promote crystallisation. Citrate and magnesium inhibit it, citrate by chelating calcium and magnesium by binding oxalate; hypocitraturia is therefore a risk factor. Calcium stones account for 70 to 80 per cent, and hypercalciuria is their commonest cause. Only 10 to 15 per cent of urinary oxalate is dietary, so restriction helps little, although oxalate-rich foods are best eaten with calcium.

Four stones, four signatures. Calcium oxalate is radio-opaque; prevention uses fluids, potassium citrate and a thiazide to lower urinary calcium. Uric acid stones are radiolucent, form in acidic urine below pH 5.5 in gout or tumour lysis, and dissolve when the urine is alkalinised to about 6.5. Struvite forms when urease-producing Proteus splits urea, alkalinises the urine and precipitates magnesium ammonium phosphate into staghorn calculi. Cure requires complete removal by percutaneous nephrolithotomy plus antibiotics. Cystine stones are faintly opaque, inherited, and managed with alkalinisation and high fluid intake. Non-contrast CT is the diagnostic standard, because every stone, including the radiolucent ones, is dense on CT. Plain films miss uric acid and cystine, and ultrasound is preferred in pregnancy and childhood.

Acute management follows three branches. A stone with fever, sepsis or a solitary obstructed kidney is an emergency: cultures, intravenous antibiotics and immediate decompression by ureteric stent or percutaneous nephrostomy, equally effective. Fragmenting the stone in an infected system drives bacteria into the circulation, so definitive treatment waits until sepsis has resolved. A stone below 5 to 6 mm without infection usually passes with observation, an NSAID in preference to opioids, and tamsulosin as medical expulsive therapy. Larger or refractory stones proceed to elective ureteroscopy or lithotripsy. Shock wave lithotripsy is contraindicated in pregnancy, uncorrected coagulopathy, an aneurysm near the stone, severe skeletal deformity and untreated infection, whereas obesity merely impairs targeting. Anticoagulated patients are best served by flexible ureteroscopy, which bleeds least.

The scrotum runs on a six-hour clock. Torsion of the spermatic cord presents with sudden severe pain and vomiting, a high-riding testis, an absent cremasteric reflex, pain unrelieved by elevation and absent Doppler flow. Salvage is high within six hours and poor beyond 24, so a convincing history goes to theatre for detorsion and bilateral fixation without waiting for imaging. Epididymitis begins gradually, elevation relieves the pain and Doppler shows increased flow. In young sexually active men the organisms are Chlamydia trachomatis and Neisseria gonorrhoeae, whereas coliforms predominate in older men. Leydig cells make testosterone under LH; Sertoli cells support spermatogenesis and secrete inhibin under FSH.

A palpable undescended testis needs no MRI. An impalpable testis is located and treated by laparoscopy; ultrasound is insensitive, and a negative scan does not prove anorchia. Orchidopexy between 6 and 18 months protects fertility and allows examination, yet the malignancy risk persists and the operation does not reduce it.

All stones with fever are drained before they are fragmented; lithotripsy in an infected system drives bacteria into the blood.
Is the stone invisible on the plain film yet bright on CT? Think uric acid, and dissolve it by alkalinising the urine to 6.5.
On the scrotum the clock runs six hours: pain worse on elevation and absent Doppler flow mean torsion and immediate exploration.
Lumbar-to-groin pain from a stone below 6 mm usually settles with an NSAID and tamsulosin, not an operation.

Embryological origin provides a useful framework for connecting a tissue’s microscopic appearance with its innervation, secretory behaviour and clinical disorders. The adrenal gland is two organs stacked together: a mesodermal cortex and a neural crest medulla. Medullary chromaffin cells are postganglionic sympathetic neurons that abandoned their axons, so preganglionic cholinergic fibres fire them directly. They release catecholamines within seconds, of which about 80 per cent is adrenaline. The cortex, by contrast, obeys humoral signals: angiotensin II and potassium for aldosterone, and ACTH for cortisol and DHEA. Pure endocrine glands have no ducts; intercalated ducts belong to salivary glands.

The same logic locates the nephron's sensors. The macula densa is a plaque of tall cells at the start of the distal tubule, against the vascular pole of its own glomerulus. It tastes luminal sodium chloride; when delivery rises, it releases adenosine, the afferent arteriole constricts and filtration falls. This tubuloglomerular feedback stops a nephron losing salt it cannot recover downstream. Renin, however, comes from juxtaglomerular cells in the afferent arteriolar wall, not from the macula densa. Examiners swap these two roles, so the anatomy must be exact.

Aristolochic acid shows how a single molecule can write two diseases. Absorbed from Aristolochia herbs such as Guan Mu Tong, it forms aristolactam-DNA adducts that leave a signature A:T to T:A transversion in TP53. The tubulointerstitium responds with paucicellular fibrosis and shrinking kidneys, and the same mutation drives urothelial carcinoma of the renal pelvis and ureter. The clinical triad is rapidly progressive renal failure, anaemia out of proportion to filtration loss, and upper tract urothelial cancer. The anaemia arrives early because erythropoietin is made by peritubular fibroblasts, the very cells that fibrosis replaces. Balkan endemic nephropathy and Chinese herb nephropathy are the same toxin in different soils. Karyomegalic interstitial nephritis reaches DNA through a FAN1 repair defect, whereas Mesoamerican nephropathy belongs to heat stress and dehydration, with no proven DNA damage.

Polycystin, the product of PKD1 and PKD2, maintains epithelial polarity, yet it also strengthens vascular smooth muscle and collagen. When it fails, the anterior circle of Willis grows berry aneurysms in 5 to 10 per cent of patients, against 2 to 3 per cent of the general population. The excess is larger in women than in men, a direction examinations like to reverse. Magnetic resonance angiography is offered after a family history of aneurysm or subarachnoid haemorrhage, for high-risk occupations, or before major surgery.

Kidney development separates builders from plumbers. The ureteric bud invades the metanephric mesenchyme, which condenses into pretubular aggregates and undergoes mesenchymal-to-epithelial transition to form tubules. Wnt4 directs that transition, with Emx2 and Fgf8 alongside; these three genes build the house. VEGF-A and its receptor Kdr lay the vascular pipes through angiogenesis and play no part in pretubular aggregation. The direction is MET, not EMT.

The central distinctions can be recalled as follows.

All chromaffin cells are neural crest neurons fired directly by preganglionic acetylcholine, releasing mainly adrenaline, whereas the mesodermal cortex answers ACTH, angiotensin II and potassium.
Is the tea an Aristolochia product? Then expect DNA adducts, TP53 transversions, paucicellular interstitial fibrosis, disproportionate anaemia and upper tract urothelial carcinoma.
On ADPKD, berry aneurysms affect 5 to 10 per cent, more often women, and MRA screening follows a family history of aneurysm or subarachnoid haemorrhage.
Luminal sodium chloride is sensed by the macula densa of the distal tubule, which releases adenosine to constrict the afferent arteriole, while juxtaglomerular cells secrete renin.

The recognition and staging of acute kidney injury depend on changes in serum creatinine and urine output, each providing a different perspective on declining renal function. The diagnosis needs a rise of 26.5 micromol per litre within 48 hours, or 1.5 times baseline within seven days. The stage follows whichever axis is worse, and starting renal replacement therapy places a patient in stage 3 whatever the creatinine. Acute tubular necrosis runs as a chain: ischaemia or a toxin kills tubular epithelium, shed cells obstruct the lumen, pressure rises, filtrate leaks back, and filtration falls into oliguria.

Localisation rests on sodium handling. Intact but underperfused tubules hoard sodium, so a prerenal state shows a fractional excretion below 1 per cent and hyaline casts. Necrotic tubules leak it, so acute tubular necrosis shows a fractional excretion above 2 per cent and muddy brown casts. In chronic kidney disease the tubule already wastes salt, so a value above 1 per cent cannot exclude a prerenal cause. Under loop diuretics a fractional excretion of urea below 35 per cent replaces it. Post-obstructive diuresis follows relief of bilateral obstruction, or obstruction of a solitary functioning kidney.

Management follows mechanism. Isotonic crystalloid restores perfusion; hydroxyethyl starch injured the tubule and raised dialysis rates in the CHEST trial. Critically ill patients are hypercatabolic and need 1.2 to 2.5 grams of protein per kilogram daily; restriction belongs to chronic disease. Urgent dialysis spells AEIOU: acidosis, electrolytes, intoxication, overload and uraemia, all refractory. Plasma exchange removes autoantibodies and paraproteins; it cannot clear potassium or acid.

Chronic kidney disease begins with phosphate retention. Osteocytes answer with FGF-23, the earliest marker to rise, which promotes phosphaturia, suppresses calcitriol and, through Klotho, restrains parathyroid hormone. As nephrons vanish, Klotho falls, that restraint breaks, and hypocalcaemia with hyperphosphataemia drives secondary hyperparathyroidism. Later the glands turn autonomous: tertiary disease. Anaemia needs iron, folate and B12 before erythropoietin. Transplantation outlives dialysis; fungal peritonitis demands immediate catheter removal; uraemic bleeding answers fastest to desmopressin; and haemodialysis does clear gadolinium.

Glomerular disease divides into nephritic and nephrotic, then by complement. Haematuria with red cell casts and hypertension marks inflammation; proteinuria above 3.5 grams a day with oedema marks a leaking podocyte barrier. Low C3 means post-infectious disease, one to three weeks after the throat, or membranoproliferative disease. Normal complement with linear IgG is anti-GBM disease, whose antigen is the alpha-3 chain of type IV collagen, whereas alpha-5 belongs to Alport syndrome. Normal complement without deposits is ANCA vasculitis; IgA nephropathy bleeds within one to three days of infection. Crescents receive high-dose corticosteroid with cyclophosphamide; anti-GBM and severe disease add plasma exchange, and rituximab equals cyclophosphamide in ANCA vasculitis. Membranous nephropathy carries the highest thrombotic risk, because antithrombin and proteins C and S leak into the urine. Renal cell carcinoma spreads by vein, renal vein to cava to right atrium, and may secrete erythropoietin or PTHrP.

The central distinctions can be recalled as follows.

All patients who start renal replacement therapy are KDIGO stage 3, and a fractional sodium excretion below 1 per cent means prerenal only when tubules are intact and diuretics absent.
Is the complement normal? Then think anti-GBM disease with linear IgG against alpha-3 collagen, or pauci-immune ANCA vasculitis, and add plasma exchange for anti-GBM.
On chronic kidney disease, FGF-23 rises first and restrains parathyroid hormone through Klotho until Klotho fails; secondary hyperparathyroidism then shows low calcium and high phosphate.
Lupus nephritis lowers both C3 and C4 with full-house immunofluorescence, whereas post-infectious disease lowers C3 alone and IgA nephropathy leaves complement normal.

A systematic acid–base assessment connects the pH, primary disturbance, expected compensation and anion gap before drawing a diagnostic conclusion. Read the pH: below 7.35 is acidaemia, above 7.45 alkalaemia. Find the primary disorder, the one that moved with the pH. Check compensation: Winter's formula predicts carbon dioxide of 1.5 times bicarbonate plus 8, and a value outside that window declares a second disorder. Then every metabolic acidosis earns an anion gap, sodium minus chloride and bicarbonate, normally 8 to 12. A raised gap means ketoacidosis, lactate, uraemia or a toxic alcohol; metformin accumulating in renal failure gives lactic acidosis without ketones. A normal gap means diarrhoea or renal tubular acidosis, split by the urine anion gap, negative in diarrhoea.

Renal tubular acidosis has three forms. Type 1 is distal failure of alpha-intercalated cells to secrete protons: urine pH stays above 5.5, potassium falls and calcium phosphate stones form. Type 2 is proximal failure to reclaim bicarbonate, often with Fanconi syndrome; the urine can still acidify. Type 4 is aldosterone deficiency or resistance, the only hyperkalaemic form. Vomiting gives a chloride-responsive alkalosis with urine chloride below 20, treated with saline and potassium.

Hyponatraemia is read in three steps. Serum osmolality comes first: glucose or mannitol draw water outward, lipid or protein create artefact, and only a low value is true. Volume comes second: hypovolaemia from gut or renal losses; euvolaemia from SIADH, hypothyroidism, adrenal insufficiency or polydipsia; hypervolaemia from heart failure, cirrhosis or nephrotic syndrome, with urine sodium below 20. Urine osmolality comes third: SIADH is euvolaemic hyponatraemia with urine osmolality above 100, urine sodium above 20 and low urea and urate. Hypertonic saline is for seizures or coma; otherwise fluid restriction leads, and correction stays within 8 to 10 mmol/L a day to avoid osmotic demyelination.

Hypokalaemia with normal urinary potassium is a shift into cells, as in periodic paralysis or insulin; above 20 is renal loss, as in diuretics, Bartter or hyperaldosteronism. Bartter mimics frusemide with normal blood pressure; Gitelman mimics a thiazide with hypomagnesaemia and hypocalciuria. Hypertension with hypokalaemia is sorted by renin and aldosterone: low renin with high aldosterone is Conn, both high is renal artery stenosis, both low is Liddle, Cushing or liquorice. Hyperkalaemia shows peaked T waves, then a wide QRS, then a sine wave. Calcium gluconate stabilises the membrane first; insulin with glucose, salbutamol and bicarbonate shift potassium inward; diuretics, binders and dialysis remove it. NSAIDs raise potassium through hyporeninaemic hypoaldosteronism; patiromer causes hypomagnesaemia.

Calcium follows phosphate. Primary hyperparathyroidism gives high calcium with low phosphate; the secondary form of chronic kidney disease gives low or normal calcium with high phosphate, FGF-23 rising first. Tertiary disease turns autonomous and calcium climbs. Hypocalcaemia lowers the threshold of excitable membranes, giving Chvostek and Trousseau signs, tetany and a long QT; hypercalcaemia depresses them into weakness, constipation and drowsiness.

The central distinctions can be recalled as follows.

All hypokalaemia is sorted by urinary potassium: normal means a shift into cells, above 20 means renal loss, Bartter mimics frusemide and Gitelman mimics a thiazide.
Is the patient euvolaemic with low serum osmolality, urine osmolality above 100 and urine sodium above 20? Then it is SIADH: restrict fluid and correct by no more than 8 to 10 mmol/L a day.
On hyperkalaemia with ECG change, calcium gluconate stabilises the myocardium first, insulin with glucose shifts potassium inward, and dialysis removes it; NSAIDs raise potassium through hyporeninaemic hypoaldosteronism.
Lungs compensate for metabolic acidosis to a carbon dioxide of 1.5 times bicarbonate plus 8, and every such acidosis earns an anion gap, normally 8 to 12.