(a) Discuss in short the aetiology, clinical features, investigations and management of chronic renal failure. (5+5+5+5=20…

(a) Chronic renal failure: aetiology, clinical features, investigations and management

Chronic renal failure (chronic kidney disease, CKD) is an irreversible, usually progressive fall in kidney function, with GFR below 60 mL/min/1.73 m² or kidney damage, for more than 3 months.

Aetiology. Diabetic nephropathy and hypertensive nephrosclerosis are the commonest; then chronic glomerulonephritis, chronic interstitial nephritis (analgesic and herbal toxins, reflux nephropathy), obstructive uropathy (stones, prostatic enlargement), adult polycystic kidney disease, lupus nephritis and, in India, CKD of unknown cause in agricultural workers.

Clinical features. They appear late, below a GFR of about 30: fatigue, anorexia, nausea, hiccups, nocturia, pruritus and a metallic taste; pallor from anaemia, oedema and hypertension; breathlessness (fluid overload, acidosis); pericarditis, uraemic frost; peripheral neuropathy, restless legs, and encephalopathy; bleeding tendency; bone pain and fractures (renal osteodystrophy); hyperkalaemia and sexual dysfunction.

Investigations. Blood urea, serum creatinine and eGFR; electrolytes (high potassium, low bicarbonate); calcium (low), phosphate and PTH (high); haemoglobin (normocytic, normochromic) and iron studies; urine analysis with albumin-creatinine ratio; ultrasound showing small echogenic kidneys (normal-sized in diabetes, polycystic disease and amyloid); renal biopsy only if kidneys are of normal size; ECG and echocardiography, and hepatitis B, C and HIV tests before dialysis.

Management. Slow progression: treat the cause; blood pressure below 130/80 with an ACE inhibitor or ARB; SGLT2 inhibitor (dapagliflozin, empagliflozin); glycaemic control; avoid NSAIDs and contrast; moderate protein (0.8 g/kg) and salt restriction; statin. Complications: iron and erythropoiesis-stimulating agents for anaemia (haemoglobin 10 to 11.5 g/dL), sodium bicarbonate for acidosis, potassium control, phosphate binders, calcium, active vitamin D and calcimimetics for bone disease. Renal replacement: haemodialysis or peritoneal dialysis when GFR is below 10 to 15 or for refractory fluid overload, hyperkalaemia, acidosis or uraemic complications, with an arteriovenous fistula made in advance. Kidney transplantation is the best option for suitable patients.

(b)(i) Causes of unconjugated hyperbilirubinaemia in the newborn

Physiological jaundice (after 24 hours, peaks day 3 to 5): high red cell load, short red cell life and immature conjugation. Increased production: Rh and ABO incompatibility and other blood group incompatibility; G6PD deficiency; hereditary spherocytosis and pyruvate kinase deficiency; polycythaemia; cephalhaematoma, bruising and swallowed blood; infant of a diabetic mother. Decreased conjugation: prematurity; Crigler-Najjar syndrome (types I and II) and Gilbert syndrome; hypothyroidism; hypoxia and acidosis; Lucey-Driscoll syndrome and breast milk jaundice. Increased enterohepatic circulation: breastfeeding jaundice from poor intake, delayed meconium, and intestinal obstruction such as pyloric stenosis. Sepsis and drugs that displace bilirubin (sulphonamides, ceftriaxone) add to the load. (Biliary atresia and neonatal hepatitis cause conjugated hyperbilirubinaemia and are not part of this list.)

(b)(ii) Mechanism of action of phototherapy

Blue-green light (wavelength 460 to 490 nm) is absorbed by bilirubin in the skin and subcutaneous tissue. It changes the molecule without conjugation in three ways: Configurational (Z to E) isomerisation, which is reversible. Structural isomerisation to lumirubin, irreversible and the main route; lumirubin is water-soluble and is excreted in bile and urine. Photo-oxidation to colourless products, a minor route. Serum bilirubin falls and the risk of kernicterus is reduced.

(b)(iii) Complications of phototherapy

Dehydration from increased insensible water loss, and loose stools; hyperthermia or hypothermia; skin rash and erythema; bronze baby syndrome (in cholestatic jaundice); retinal damage if the eyes are not shielded; hypocalcaemia and increased haemolysis in some preterm babies; and disturbed mother-baby bonding.

(c)(i) Nail findings in psoriasis

Pitting (the commonest, from the nail matrix); oil-drop or salmon-patch discolouration (nail bed); onycholysis; subungual hyperkeratosis; splinter haemorrhages; crumbling nail dystrophy and leukonychia; red spots in the lunula. Nail change is seen in about half of the patients and is common in psoriatic arthritis.

(c)(ii) Topical and systemic therapy of psoriasis

Topical (for limited disease, under 10% of body surface): Emollients, keratolytics (salicylic acid) and coal tar. Dithranol for plaques. Corticosteroids: potency graded by site (mild on face and flexures, potent on trunk and limbs, super-potent on palms and soles), short courses to avoid atrophy and rebound. Vitamin D analogues (calcipotriol, calcitriol), the calcipotriol and betamethasone combination, and tazarotene. Calcineurin inhibitors (tacrolimus) on face and folds.

Systemic (for extensive disease, PASI or DLQI above 10, special sites or failure of topical therapy): Phototherapy (narrow-band UVB, PUVA). Methotrexate weekly with folic acid (monitor blood counts and liver); ciclosporin (monitor blood pressure and creatinine, limited to a year); acitretin (teratogenic, avoid in women who may conceive). Apremilast, and newer oral agents such as tofacitinib and deucravacitinib. Biologics: TNF-α inhibitors (adalimumab, etanercept, infliximab), IL-12/23 (ustekinumab), IL-17 inhibitors (secukinumab, ixekizumab) and IL-23 inhibitors (guselkumab, risankizumab). Screen for tuberculosis and hepatitis B before biologics.