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

Chronic renal failure. Chronic renal failure is the irreversible loss of renal function, now framed as CKD when structural or functional abnormality persists for >3 months. In India, diabetic nephropathy and hypertensive nephrosclerosis are the commonest aetiologies, followed by chronic glomerulonephritis, chronic interstitial nephritis, obstructive uropathy and polycystic kidney disease; late presentation is common because of limited access to screening. CKD is staged by eGFR: stage 1 ≥90 mL/min/1.73 m² with kidney damage; stages 2–5 are 60–89, 45–59, 30–44, 15–29 and <15 mL/min/1.73 m² respectively. Staging guides prognosis, drug dosing and referral. Clinical features reflect uraemia: anorexia, nausea, fatigue, pruritus, metallic taste, pericarditis, encephalopathy, bleeding due to platelet dysfunction, anaemia from reduced erythropoietin, metabolic acidosis, hyperphosphataemia, hypocalcaemia and renal osteodystrophy. Investigations include serum creatinine/eGFR, electrolytes, ABG, calcium/phosphate/PTH, haemoglobin, urinalysis, renal ultrasound, and biopsy when glomerular disease is suspected. Management is aetiological and supportive: control BP with ACE inhibitor/ARB where appropriate, glycaemic control, treat anaemia, acidosis, mineral-bone disorder, and avoid nephrotoxins. Renal replacement therapy is needed in stage 5 or with refractory uraemia, hyperkalaemia, acidosis or fluid overload: haemodialysis, peritoneal dialysis or continuous renal replacement in unstable patients; dialysis planning should include vascular access, patient education and psychosocial support. Kidney transplantation is the preferred long-term option when immunologically suitable, with compatible HLA/crossmatch and no active infection, malignancy or uncontrolled disease.

Neonatal unconjugated hyperbilirubinaemia. In a newborn, unconjugated hyperbilirubinaemia may be physiological, due to increased red cell mass, short RBC survival and immature hepatic conjugation. Pathological causes include haemolysis from ABO/Rh incompatibility, hereditary spherocytosis, G6PD deficiency—important in India—sepsis, cephalohaematoma, and inborn errors such as Crigler-Najjar syndrome. Breast milk jaundice, hypothyroidism, and galactosaemia can also raise unconjugated bilirubin. Management follows NICE/Indian Academy of Pediatrics principles: assess risk, serial bilirubin, early feeding, hydration and temperature monitoring, and treat with phototherapy or exchange transfusion when thresholds are crossed. Phototherapy is first-line; exchange transfusion prevents kernicterus.

Phototherapy. Phototherapy works by photoisomerisation of unconjugated bilirubin in the skin into water-soluble lumirubin and configurational isomers, which are excreted in bile and urine without hepatic conjugation. It reduces serum unconjugated bilirubin and risk of bilirubin neurotoxicity. It is effective for unconjugated, not conjugated, bilirubin. Blue light, eye shielding, continuous exposure, hydration and temperature monitoring are essential. Potential complications include dehydration and heat loss, temperature instability, skin rash, retinal damage if eyes are not shielded, and bronze baby syndrome when conjugated bilirubin is also present.

Psoriasis. Nail psoriasis shows pitting, oil-drop or salmon-patch discolouration of the nail bed, onycholysis, subungual hyperkeratosis, and splinter haemorrhages; these reflect matrix and nail-bed inflammation. Topical therapy is first-line for limited disease: potent corticosteroids, vitamin D analogues such as calcipotriol, dithranol, coal tar, keratolytics and emollients; combination calcipotriol/betamethasone is useful for plaques and nails. Topical therapy should be combined with emollients and occlusion; systemic therapy requires shared decision-making. Systemic therapy is considered for extensive, rapidly progressive, or disabling disease, using PASI, BSA and DLQI to gauge severity. Conventional agents include methotrexate, cyclosporine and acitretin. Biologics now transform care: anti-TNF agents (adalimumab, etanercept), IL-17 inhibitors (secukinumab, ixekizumab), IL-23 inhibitors such as guselkumab, and the IL-12/23 inhibitor ustekinumab. Choice depends on comorbidities, infection risk, pregnancy plans, cost and access in India. Methotrexate needs CBC/LFT monitoring, cyclosporine BP/creatinine surveillance, acitretin lipid monitoring, and biologics require TB screening.

Way forward. These conditions require staged, guideline-based care: CKD needs early nephrology referral, dialysis planning and transplant evaluation; neonatal jaundice needs timely risk assessment and safe phototherapy; psoriasis needs integrated skin, nail and systemic management with monitoring. In India, strengthening primary screening for CKD, neonatal bilirubin protocols, and affordable biologic access will improve outcomes.