Quick Answer
Chronic kidney disease is a 3 to 4 question topic per NEET PG paper. Lock these:
- KDIGO CGA staging — G1 to G5 by eGFR, A1 to A3 by albuminuria; both matter for prognosis.
- Etiology in India — diabetic nephropathy leads; then hypertensive nephrosclerosis; CKDu in Andhra-Odisha coastal belt.
- SGLT2 inhibitors — DAPA-CKD and EMPA-KIDNEY; now first-line in proteinuric CKD, diabetic or not.
- RAAS blockade — ACEi/ARB for proteinuric CKD; accept up to 30 percent eGFR drop; monitor potassium.
- Finerenone — non-steroidal MRA (FIDELIO-DKD) for diabetic CKD with residual proteinuria.
- CKD-MBD — phosphate binders (non-calcium preferred), calcimimetics, vitamin D analogues.
- Anaemia — iron first, then ESA; target Hb 10 to 11.5 (do NOT normalise).
- RRT indications (AEIOU) — Acidosis, Electrolyte, Ingestion, Overload, Uraemia.
- Modalities — HD (AVF preferred, catheter last), PD (CAPD/APD; peritonitis Staph epidermidis), transplant (best outcome, pre-emptive from living donor).
- Indian programmes — PMNDP, Ayushman Bharat PM-JAY, NPCDCS, NOTTO, HOTA 1994.
Chronic kidney disease is a growing epidemic in India — the combination of the world's largest diabetic population (over 100 million), one of the highest hypertension prevalences, and a distinctive belt of CKD of unknown etiology in coastal Andhra Pradesh and Odisha (Uddanam nephropathy) makes CKD one of the fastest-growing burdens on the Indian health system. NEET PG tests CKD across nephrology, internal medicine, community medicine (PMNDP), and surgery (vascular access, transplantation).
This NEETPGAI deep dive walks through KDIGO staging → complications and their targeted management → RAAS/SGLT2i/finerenone → nephrology referral → RRT modalities → transplantation → India programmatic context. Pair this with the diabetes mellitus complications guide and the hypertension management guide for the medicine cluster.
Defining and staging CKD
Definition (KDIGO 2012)
Abnormalities of kidney structure or function present for greater than 3 months with implications for health. Requires ONE of:
- eGFR less than 60 mL/min per 1.73 m squared for greater than 3 months, OR
- Markers of kidney damage — albuminuria (ACR at least 30 mg/g), urinary sediment abnormalities (haematuria), electrolyte or tubular disorders, histology on biopsy, structural abnormalities on imaging (polycystic kidneys, obstruction, reflux), or history of kidney transplantation
GFR staging (G1 to G5)
| Stage | eGFR (mL/min/1.73 m squared) | Description |
|---|
| G1 | greater than 90 | Normal or high (with damage marker to qualify as CKD) |
| G2 | 60-89 | Mildly decreased (with damage marker) |
| G3a | 45-59 | Mild to moderately decreased |
| G3b | 30-44 | Moderately to severely decreased |
| G4 | 15-29 | Severely decreased |
| G5 | less than 15 | Kidney failure (or on dialysis) |
Albuminuria staging (A1 to A3)
| Stage | ACR (mg/g) | 24-hour albuminuria | Old terminology |
|---|
| A1 | less than 30 | less than 30 mg/day | Normal to mildly increased |
| A2 | 30-300 | 30-300 mg/day | Moderately increased (microalbuminuria) |
| A3 | greater than 300 | greater than 300 mg/day | Severely increased (macroalbuminuria) |
The KDIGO heatmap combines GFR and albuminuria into a colour-coded risk grid — a patient with eGFR 55 and ACR 250 (G3a A2) is at high risk despite an eGFR that looks nearly normal.
Etiology in India
| Etiology | Approximate share | Notes |
|---|
| Diabetic nephropathy | 40-45 percent | Most common; parallels India's diabetic epidemic |
| Hypertensive nephrosclerosis | 20-25 percent | Second most common |
| Chronic glomerulonephritis | 10-15 percent | Primary (IgA, FSGS, membranous) and secondary (lupus, HBV, HCV) |
| Obstructive uropathy | 5-10 percent | BPH, stones, malignancy |
| Polycystic kidney disease | 5 percent | ADPKD; family history |
| Chronic tubulointerstitial disease | 5-10 percent | Analgesic nephropathy, reflux, heavy-metal exposure |
| CKD of unknown etiology (CKDu) | Regional | Uddanam nephropathy in coastal Andhra-Odisha; young men, agricultural workers, no diabetes or hypertension |
| Drug-induced | 5-10 percent | NSAIDs (long-term chronic use), aminoglycosides, cisplatin, calcineurin inhibitors, contrast |
Pathophysiology of progression
The hyperfiltration hypothesis — as nephrons are lost (from any initial insult), the remaining nephrons compensate by increasing single-nephron GFR (via afferent vasodilatation and efferent vasoconstriction driven by angiotensin II). This chronic glomerular hypertension damages the podocyte and endothelium, producing proteinuria and further nephron loss — a feed-forward cycle. This mechanism explains why:
- Proteinuria is both a marker AND a driver of progression
- ACE inhibitors and ARBs slow progression by reducing efferent arteriolar tone and intraglomerular pressure
- SGLT2 inhibitors slow progression by restoring tubuloglomerular feedback and reducing intraglomerular pressure from the afferent side
Uremic toxins — small molecules (urea, creatinine, uric acid), middle molecules (beta-2 microglobulin), and protein-bound solutes (indoxyl sulphate, p-cresyl sulphate) accumulate and drive symptoms and cardiovascular risk.
Clinical features by stage
| Stage | Clinical features |
|---|
| G1-G2 | Usually asymptomatic; picked up on screening (proteinuria, haematuria, imaging) |
| G3a | Usually asymptomatic; mild anaemia, mild secondary hyperparathyroidism start |
| G3b | Fatigue from anaemia, restless legs, mild uraemia; hypertension worsens |
| G4 | Uraemic symptoms (nausea, poor appetite), pruritus, restless legs, sleep disturbance, mild encephalopathy, fluid overload; prepare for RRT (vascular access, transplant workup) |
| G5 | Overt uraemia — nausea and vomiting, uraemic frost, pericarditis, encephalopathy with asterixis, fluid overload, hyperkalaemia; initiate RRT on symptoms |
Complications — targeted management
1) Anaemia
- Cause — reduced erythropoietin (EPO) production by peritubular fibroblasts + absolute or functional iron deficiency + shortened RBC lifespan in uraemia + inflammation (raised hepcidin)
- Investigations — CBC, iron studies (ferritin and transferrin saturation), reticulocyte count; exclude other causes (haemolysis, GI blood loss)
- Management — repleted iron first (oral if tolerable, IV iron sucrose or ferric carboxymaltose if not; target ferritin greater than 100 ng/mL and TSAT greater than 20 percent), then erythropoiesis-stimulating agents (epoetin alfa, darbepoetin) starting once Hb less than 10 g/dL
- Target Hb 10 to 11.5 g/dL — do NOT normalise; TREAT, CHOIR, and CREATE trials showed higher cardiovascular events and stroke risk with a haemoglobin target above 13 g/dL
- HIF stabilisers (roxadustat, daprodustat) — newer oral agents; used in some Indian centres
2) CKD-MBD (Mineral and Bone Disorder)
- Axis — phosphate rises (retention) → FGF-23 rises → calcitriol falls → serum calcium falls → PTH rises (secondary hyperparathyroidism); chronic secondary can become autonomous tertiary hyperparathyroidism
- Vascular calcification — a major cardiovascular risk driver in CKD; drives coronary and peripheral vascular disease
- Phosphate control — dietary phosphate restriction; phosphate binders taken with meals
- Calcium-based binders (calcium carbonate, calcium acetate) — cheap but risk hypercalcaemia and vascular calcification
- Non-calcium binders (sevelamer, lanthanum) — preferred if evidence of vascular calcification or hypercalcaemia
- Iron-based binders (ferric citrate, sucroferric oxyhydroxide) — newer; also treat iron deficiency
- Calcium — target 8.4-9.5 mg/dL; avoid hypercalcaemia
- Vitamin D — supplement cholecalciferol for 25-OH-D less than 30 ng/mL; add active analogues (calcitriol, paricalcitol) for persistent hyperparathyroidism
- Calcimimetics — cinacalcet (oral), etelcalcetide (IV during dialysis) — for refractory secondary hyperparathyroidism
- Parathyroidectomy — subtotal or total with autotransplant to the forearm for medically refractory tertiary hyperparathyroidism, hypercalcaemia, or intractable pruritus/bone pain
3) Metabolic acidosis
- Cause — reduced ammoniagenesis and bicarbonate regeneration
- Consequences — muscle wasting, bone demineralisation, faster CKD progression
- Management — sodium bicarbonate 0.5-1 mmol/kg/day PO to keep serum bicarbonate greater than 22 mmol/L; monitor sodium load and BP
4) Fluid overload and hypertension
- Salt restriction less than 5 g/day (about 2 g of sodium)
- Loop diuretics — furosemide or torsemide; higher doses needed as GFR falls
- BP target less than 120 systolic (SPRINT trial — CKD subgroup showed cardiovascular benefit); individualise for elderly, orthostasis, hyperkalaemia risk
- RAAS blockade as first-line for proteinuric CKD (see below)
5) Hyperkalaemia
- Dietary restriction — reduce bananas, oranges, potatoes, tomatoes, coconut water; leach potatoes if used
- Loop diuretics — kaliuretic
- Sodium bicarbonate — corrects acidosis, shifts K into cells
- Potassium binders — patiromer (calcium-based, oral) and sodium zirconium cyclosilicate (ZS-9) — newer, better tolerated than SPS (sodium polystyrene sulphonate, kayexalate) which has fallen out of favour due to bowel necrosis risk
- Emergency hyperkalaemia — calcium gluconate (cardiac protection), insulin-glucose or nebulised salbutamol (shift into cells), then dialysis if persistent
6) Uraemic pruritus
- Antihistamines usually ineffective; use gabapentin, pregabalin, moisturisers, difelikefalin (newer kappa-opioid receptor agonist), phototherapy; parathyroidectomy for hyperparathyroidism-driven pruritus
Slowing progression — RAAS, SGLT2i, finerenone
RAAS blockade (ACE inhibitors, ARBs)
- Indication — proteinuric CKD (ACR greater than 30 mg/g); hypertensive CKD; diabetic nephropathy
- Mechanism — efferent arteriolar vasodilatation reduces intraglomerular pressure and proteinuria
- Accept up to 30 percent eGFR drop in the first 2-4 weeks as a haemodynamic effect — greater drops warrant investigation for volume depletion or renal artery stenosis
- Monitor potassium and creatinine at 2-4 weeks and after each dose change
- Contraindications — bilateral renal artery stenosis, pregnancy, hyperkalaemia
- Do NOT combine ACEi + ARB (ONTARGET showed harm) or add aliskiren
SGLT2 inhibitors
- DAPA-CKD (dapagliflozin) — diabetic and non-diabetic proteinuric CKD, eGFR 25-75, ACR 200-5000; reduced eGFR decline and mortality
- EMPA-KIDNEY (empagliflozin) — broader CKD population including non-proteinuric; benefit confirmed
- Mechanism — restore tubuloglomerular feedback (increased NaCl to macula densa → afferent vasoconstriction → reduced intraglomerular pressure); glycosuria, natriuresis, mild volume reduction; benefit is largely non-glycaemic
- Threshold — dapagliflozin can be initiated down to eGFR 20; empagliflozin down to eGFR 25; both are continued to dialysis initiation
- Adverse effects — genital mycotic infections, euglycaemic DKA (in diabetics — hold during acute illness and 3 days pre-surgery), mild volume depletion, initial 3-5 mL/min eGFR dip (haemodynamic, expected)
Finerenone (non-steroidal MRA)
- FIDELIO-DKD and FIGARO-DKD — reduces composite renal and cardiovascular endpoints in diabetic CKD with residual proteinuria on RAAS
- Advantage over spironolactone — greater selectivity for mineralocorticoid receptor, less risk of gynaecomastia; lower hyperkalaemia risk than spironolactone at equivalent renal effect
- Monitor potassium — hold or reduce dose if potassium greater than 5.5
Glycemic control in CKD
- Metformin is safe down to eGFR 30 (avoid below eGFR 30 — lactic acidosis risk)
- SGLT2 inhibitors preferred (see above)
- GLP-1 receptor agonists (semaglutide, liraglutide, dulaglutide) — safe and cardio-renal beneficial in CKD
- Sulfonylureas — avoid glibenclamide (long-acting, hypoglycaemia risk in CKD); glipizide or glimepiride safer
- Insulin — reduce dose as GFR falls (renal insulin clearance drops); risk of hypoglycaemia
Renal replacement therapy (RRT)
When to initiate (AEIOU absolute indications)
- A — Acidosis (refractory metabolic acidosis)
- E — Electrolyte imbalance (refractory hyperkalaemia)
- I — Ingestion (dialysable toxin — methanol, ethylene glycol, lithium)
- O — Overload (refractory fluid overload with pulmonary oedema)
- U — Uraemia (uraemic pericarditis, encephalopathy, bleeding, intractable nausea)
- Also refractory hyponatraemia and refractory hypocalcaemia
The IDEAL trial showed no mortality difference between eGFR 10-14 (early) and eGFR 5-7 (late) initiation — decision should be symptom-driven, not eGFR-driven.
Haemodialysis (HD)
- Access options (in decreasing preference):
- Arteriovenous fistula (AVF) — best long-term patency and lowest infection risk; requires 6-12 weeks to mature; created on non-dominant arm typically radiocephalic (Brescia-Cimino), then brachiocephalic, then brachiobasilic transposition
- Arteriovenous graft (AVG) — synthetic PTFE; useful when native veins are inadequate; higher thrombosis and infection than AVF
- Tunnelled central venous catheter (Permcath) — for bridging; higher infection and central-vein stenosis
- Non-tunnelled catheter — for emergency dialysis only; remove as soon as possible
- Vein preservation — no peripheral IVs, no blood draws, no BP cuff on the future access arm; this is a critical care-team responsibility from the moment CKD is diagnosed
- Modality — in-centre thrice-weekly HD; home HD in select patients; nocturnal HD; slow low-efficiency dialysis (SLED) for haemodynamically unstable patients
- Complications — hypotension (most common), muscle cramps, disequilibrium syndrome (first sessions in severe uraemia), access thrombosis, access infection (Staph aureus most common), amyloidosis (β2-microglobulin, carpal tunnel), heparin-induced thrombocytopenia
Peritoneal dialysis (PD)
- CAPD (continuous ambulatory PD) — 4 exchanges daily by the patient; volume 2-2.5 L per exchange
- APD (automated PD) — nocturnal cycler; convenient for working patients and children
- Advantages — home therapy, preserves residual renal function longer, better haemodynamic stability, no vascular access needed
- Disadvantages — protein loss (higher dietary protein needed, 1.2-1.5 g/kg/day), peritoneal fibrosis with long-term use, encapsulating peritoneal sclerosis (rare, feared)
- PD peritonitis — the main complication; classic diagnosis by cloudy effluent with WCC greater than 100/microlitre and greater than 50 percent PMNs
- Staphylococcus epidermidis is the most common organism (skin contamination during exchanges)
- Staph aureus (tunnel infection), Streptococcus, Gram-negatives (Pseudomonas), fungi (Candida) also occur
- Empiric therapy — intraperitoneal cefazolin (Gram-positive cover) plus ceftazidime or gentamicin (Gram-negative cover); tailor to culture
Kidney transplantation
- Best outcome modality for medically eligible patients
- Pre-emptive transplant (before starting dialysis) has the best long-term outcomes
- Donor options:
- Living donor — first-degree relatives (parents, siblings, spouse, children) — legal in India under HOTA 1994 without authorisation committee for close relatives; better graft survival than deceased donor
- Deceased donor (brain-death) — regulated by NOTTO; India's brain-death programme is limited by cultural and religious factors
- HLA matching — ABO compatibility is required; HLA matching (A, B, DR) improves outcomes; DR mismatch matters most; paired donor exchange (KPD) for ABO-incompatible pairs
- Immunosuppression — triple therapy standard: calcineurin inhibitor (tacrolimus preferred over cyclosporine) + antimetabolite (mycophenolate mofetil preferred over azathioprine) + steroid (prednisolone, often tapered); induction with basiliximab or anti-thymocyte globulin
- Rejection:
- Hyperacute (minutes to hours) — pre-formed donor-specific antibodies; ABO mismatch; results in graft loss; prevented by cross-match
- Acute cellular rejection (weeks to months) — T-cell mediated; treated with pulse steroids; biopsy diagnosis with tubulitis
- Antibody-mediated rejection (AMR) — donor-specific antibodies; treated with plasmapheresis, IVIG, rituximab
- Chronic allograft injury (CAI) — years; progressive fibrosis and dysfunction; multifactorial (donor factors, antibody, calcineurin nephrotoxicity)
- Post-transplant complications — infections (CMV, BK virus, Pneumocystis, TB — endemic in India), malignancy (skin cancer, PTLD from EBV), diabetes (NODAT), cardiovascular disease, calcineurin inhibitor toxicity
Nutrition in CKD
- Pre-dialysis (G3-G5 not yet on RRT) — protein 0.8 g/kg/day; sodium less than 2 g/day; phosphate restriction; potassium restriction as needed
- Haemodialysis — protein 1.2 g/kg/day (higher because dialysis clears amino acids)
- Peritoneal dialysis — protein 1.2-1.5 g/kg/day (higher because significant protein lost in dialysate)
- Adequate energy intake (30-35 kcal/kg/day) to prevent protein-energy wasting
India-specific programmatic context
- Pradhan Mantri National Dialysis Programme (PMNDP) — launched 2016 under NHM; provides free HD at district hospital dialysis units to BPL patients; over 1500 centres and growing; adds transport support
- Ayushman Bharat PM-JAY — up to Rs 5 lakh per family per year for secondary and tertiary care including dialysis and transplantation in empanelled hospitals
- State schemes — Amma Dialysis (Tamil Nadu), Aarogyasri (Telangana/Andhra), Karunya (Kerala), Biju Krushak Kalyan Yojana (Odisha)
- NPCDCS — screens and manages hypertension and diabetes at primary care level; upstream CKD prevention
- NOTTO/ROTTO/SOTTO — three-tier organ allocation network under HOTA 1994
- HOTA (Human Organ Transplantation Act 1994, amended 2011) — legal framework; permits living-donor first-degree-relative transplant without review committee; other living donors require authorisation committee; commerce prohibited; brain-death donation allowed
- CKDu (Uddanam nephropathy) in Andhra-Odisha coastal belt — cause unknown; hypotheses include heat stress in agricultural workers, environmental toxins, dehydration-driven tubular injury; NPCDCS + regional research ongoing
NEET PG MCQ traps
- KDIGO stage — G1 to G5 by eGFR + A1 to A3 by ACR; both matter (CGA classification).
- G3a vs G3b — split at eGFR 45.
- eGFR less than 60 for greater than 3 months = CKD by definition.
- Albuminuria — ACR at least 30 mg/g qualifies as kidney damage marker.
- Most common cause of CKD in India — diabetic nephropathy.
- CKDu Uddanam nephropathy — coastal Andhra-Odisha; young agricultural workers.
- DAPA-CKD and EMPA-KIDNEY — SGLT2i in proteinuric CKD, diabetic and non-diabetic.
- RAAS blockade — accept 30 percent eGFR drop; monitor K; do NOT combine ACEi + ARB.
- Finerenone — non-steroidal MRA (FIDELIO-DKD) for diabetic CKD with residual proteinuria.
- Metformin — safe down to eGFR 30; avoid below.
- Anaemia target Hb 10 to 11.5 g/dL — do NOT normalise (TREAT, CHOIR).
- Iron first, then ESA — target ferritin greater than 100, TSAT greater than 20.
- Phosphate binders — non-calcium (sevelamer, lanthanum, ferric citrate) preferred for vascular calcification.
- Cinacalcet — calcimimetic for refractory secondary hyperparathyroidism.
- Parathyroidectomy — refractory tertiary hyperparathyroidism.
- Sodium bicarbonate — target serum bicarbonate greater than 22.
- Potassium binders — patiromer, ZS-9 (SPS falling out of favour due to bowel necrosis).
- AEIOU — indications for urgent dialysis initiation.
- IDEAL trial — early vs late dialysis start — no mortality difference.
- Vascular access — AVF preferred; AVG next; catheter last resort.
- AVF maturation — 6-12 weeks; plan 3-6 months before need.
- PD peritonitis — Staph epidermidis most common (skin contamination during exchanges).
- Best transplant outcome — pre-emptive living-donor.
- Tacrolimus + mycophenolate + steroid — standard immunosuppression.
- Hyperacute rejection — preformed antibodies (ABO mismatch); minutes to hours.
- PMNDP — launched 2016; free HD at district hospitals.
- HOTA 1994 (amended 2011) — first-degree relatives without review committee.
- NOTTO — national organ allocation network.
- Pregnancy in CKD — hold ACEi/ARB, SGLT2i, mycophenolate.
- CKD-MBD — vascular calcification is the CV risk driver.
Recent updates and Indian context
- DAPA-CKD (2020) and EMPA-KIDNEY (2023) trials — SGLT2 inhibitors now standard of care in proteinuric CKD, diabetic and non-diabetic; endorsed in KDIGO 2022 and 2024 updates
- FIDELIO-DKD and FIGARO-DKD (2020-2021) — finerenone in diabetic CKD with residual proteinuria despite RAAS
- HIF-PHI inhibitors (roxadustat, daprodustat) — approved in Asia for CKD anaemia; oral alternative to ESA; being adopted in Indian tertiary centres
- Potassium binders — patiromer and sodium zirconium cyclosilicate (ZS-9) available in India; enable RAAS titration by preventing hyperkalaemia
- Difelikefalin — kappa-opioid agonist for CKD-associated pruritus (approved 2021, US)
- Kidney xenotransplantation research (pig-to-human) — early clinical trials; not yet clinical routine
- PMNDP expansion — over 1500 dialysis units nationally; catchment expanded to community health centre level in some states
- Chronic kidney disease of unknown etiology (CKDu) research — collaboration between AIIMS, NIMS, and ICMR on Uddanam nephropathy; heat-stress and environmental-toxin hypotheses under investigation
Frequently asked questions
How does KDIGO 2012 stage CKD and what does the CGA classification mean?
KDIGO 2012 defines CKD as abnormalities of kidney structure or function present for over 3 months with implications for health. Staging uses the CGA classification — Cause (C), GFR (G), and Albuminuria (A). GFR staging G1 to G5 is by eGFR (mL/min per 1.73 m squared) — G1 greater than 90 with kidney damage marker, G2 60-89 with damage marker, G3a 45-59, G3b 30-44, G4 15-29, G5 less than 15 (or dialysis). Albuminuria staging A1 to A3 is by urine albumin-to-creatinine ratio — A1 less than 30 mg/g (normal to mildly increased), A2 30-300 mg/g (moderately increased, previously called microalbuminuria), A3 greater than 300 mg/g (severely increased, previously called macroalbuminuria). Prognosis is a colour-coded heatmap of GFR versus albuminuria — green (low risk) to red (very high risk). A patient with eGFR 50 mL/min and ACR 200 mg/g is G3a A2, which is high risk irrespective of the eGFR alone. NEET PG most commonly tests the eGFR thresholds, the ACR thresholds, and the point that albuminuria is an independent risk modifier — a patient with normal eGFR but heavy proteinuria still has CKD.
Why are SGLT2 inhibitors now first-line in proteinuric CKD irrespective of diabetes?
The DAPA-CKD and EMPA-KIDNEY trials proved that SGLT2 inhibitors reduce the composite of eGFR decline, ESKD, cardiovascular death, and hospitalisation for heart failure in proteinuric CKD, in both diabetic and non-diabetic patients. Mechanistically SGLT2 inhibitors restore tubuloglomerular feedback by increasing sodium delivery to the macula densa, causing afferent arteriolar vasoconstriction, reducing intraglomerular pressure and hyperfiltration — the same protective principle as RAAS blockade acting on the efferent side, but from the afferent side. The result is an initial eGFR dip of 3-5 mL/min (haemodynamic, reversible) followed by a much slower long-term decline than placebo. Indications now include diabetic and non-diabetic proteinuric CKD with eGFR down to 20 mL/min (dapagliflozin) or 25 mL/min (empagliflozin) — do not start below these thresholds. Adverse effects to counsel — genital mycotic infections, euglycaemic DKA (in diabetics — hold during acute illness and surgery), a small volume-depletion effect. NEET PG has begun testing DAPA-CKD and EMPA-KIDNEY explicitly since 2023-2024.
What is CKD-MBD and how do you manage the calcium-phosphate-PTH-vitamin D axis?
Chronic kidney disease mineral and bone disorder (CKD-MBD) is the systemic disorder involving biochemical abnormalities (calcium, phosphate, PTH, vitamin D, FGF-23), bone abnormalities (renal osteodystrophy — high-turnover, low-turnover, mixed, or adynamic bone disease), and vascular/soft-tissue calcification (a major cardiovascular risk driver in CKD). The pathophysiology cascade — as GFR falls, phosphate excretion falls, FGF-23 rises to compensate, calcitriol production falls, calcium absorption falls, PTH rises (secondary hyperparathyroidism) to compensate; chronically autonomous parathyroid glands become tertiary hyperparathyroidism. Management targets — phosphate less than 5.5 mg/dL (dietary restriction plus phosphate binders — calcium-based sevelamer or lanthanum for non-calcium; iron-based ferric citrate or sucroferric oxyhydroxide as newer options); calcium 8.4-9.5 mg/dL (correct hypocalcaemia but avoid hypercalcaemia and calcium load — vascular calcification); PTH 2 to 9 times the upper limit of normal on dialysis (do not over-suppress — adynamic bone disease); vitamin D — repletion with cholecalciferol for 25-OH-D less than 30 ng/mL, active vitamin D analogues (calcitriol, paricalcitol) for persistent secondary hyperparathyroidism; calcimimetics (cinacalcet oral, etelcalcetide IV) for refractory secondary hyperparathyroidism. Parathyroidectomy (subtotal or total with autotransplant) for medically refractory tertiary hyperparathyroidism. NEET PG most commonly tests the phosphate binder choices, the vitamin D options, and the fact that calcium-based binders are being replaced by non-calcium binders because of vascular calcification concerns.
When should CKD be referred to nephrology and when should RRT be initiated?
Nephrology referral is indicated at eGFR less than 30 mL/min (KDIGO stage G4-G5), rapid progression (eGFR decline greater than 5 mL/min per year), resistant hypertension (uncontrolled on 3 drugs including a diuretic), resistant anaemia despite iron repletion, refractory electrolyte abnormalities (hyperkalaemia, acidosis), CKD-MBD not controlled by primary care, unexplained haematuria or heavy proteinuria (ACR greater than 300 mg/g), and any diagnostic uncertainty. Early referral improves outcomes — vascular access can be planned, transplant work-up can start, patient can be educated. RRT initiation is a clinical, not a lab-value, decision — the IDEAL trial showed that early (eGFR 10-14) versus late (eGFR 5-7) start of dialysis did not change mortality. Initiate on symptoms rather than an eGFR number — uraemic symptoms (nausea, anorexia, weight loss, pruritus, uraemic encephalopathy, uraemic pericarditis, uraemic bleeding), refractory fluid overload despite diuretics, refractory hyperkalaemia, refractory metabolic acidosis, or failed conservative management. Absolute indications (AEIOU) — Acidosis, Electrolyte imbalance (hyperkalaemia), Ingestion of toxins, Overload (fluid), Uraemia (pericarditis, encephalopathy). Modality choice is guided by patient preference, home support, comorbidity, and access; transplant (preferably pre-emptive from a living donor) gives the best outcomes.
What Indian government programmes cover CKD, dialysis and transplantation?
India carries one of the world's largest CKD burdens driven by diabetes, hypertension, and CKD of unknown etiology (CKDu) in the Andhra-Odisha coastal belt (Uddanam nephropathy). Government financing includes (1) Pradhan Mantri National Dialysis Programme (PMNDP) launched 2016 under National Health Mission — provides free haemodialysis at district hospital dialysis units to BPL patients; over 1500 centres and rising; adds transportation support. (2) Ayushman Bharat PM-JAY — up to Rs 5 lakh per family per year for secondary and tertiary care including dialysis, transplant, and post-transplant follow-up in empanelled hospitals; covers a substantial portion of Indian CKD population. (3) State-level programmes — Amma Dialysis in Tamil Nadu, Aarogyasri in Telangana and Andhra Pradesh, Karunya scheme in Kerala. (4) NPCDCS (National Programme for Prevention and Control of Cancers, Diabetes, CVD and Stroke) — screens and manages hypertension and diabetes at the primary care level, upstream CKD prevention. (5) NOTTO (National Organ and Tissue Transplant Organisation) — regulates transplantation, allocation, and donor registration; brain-death donor programme is limited by cultural factors. (6) HOTA (Human Organ Transplantation Act, 1994, amended 2011) — legal framework; permits living-donor first-degree-relative transplants without a review committee and other living donors with authorisation committee approval; prohibits organ commerce. Transplantation numbers remain far below need — India performs ~10,000 kidney transplants per year against a projected requirement of over 200,000, so peritoneal dialysis and haemodialysis absorb most of the burden.
This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: July 2026
