What Is Chronic Kidney Disease (CKD) — Stages, Symptoms, and When to See a Nephrologist
Chronic kidney disease (CKD) is a condition in which the kidneys gradually lose their filtering ability over months or years a slow, progressive decline that often produces no symptoms until significant function has already been lost. In India, CKD affects an estimated 17% of the adult population to some degree. Diabetes and hypertension both extraordinarily prevalent in Telangana and Andhra Pradesh account for more than half of all CKD cases. The cruel irony of CKD is that the kidneys' enormous reserve capacity means that a person can lose more than 60% of kidney function before experiencing any symptoms at all. By the time symptoms appear, meaningful damage has already occurred.
This is why understanding CKD — what it is, what causes it, how it is staged, and when specialist review is essential is the most important piece of kidney health education for the Indian population. Early CKD, identified by blood and urine tests at a routine check-up, is manageable and its progression can be significantly slowed with the right interventions. Late-stage CKD, presenting with breathlessness, swelling, nausea, and profound fatigue, represents a much narrower window for intervention before dialysis or transplant becomes necessary.
At KIMS Secunderabad, CKD management is led by a team of DM Nephrology-qualified specialists who provide care across the entire CKD trajectory from the first detected abnormality in kidney function (a raised serum creatinine on a routine check, or protein in the urine on a diabetes review) through to dialysis initiation and kidney transplant where needed. The same nephrologist who first detects and treats early CKD continues to manage the patient through every subsequent stage — no referrals to a different team, no restart of medical history at each transition.
How the kidneys work — and what happens when they fail
The kidneys are two fist-sized organs, one on each side of the spine behind the abdominal cavity, that filter approximately 180 litres of blood per day. Every minute, about 1.2 litres of blood passes through the kidneys' filtering units (glomeruli), where waste products, excess fluid, and electrolytes are removed into the urine while proteins, blood cells, and essential molecules are retained in the circulation. The kidneys also regulate blood pressure (through the renin-angiotensin system), stimulate red blood cell production (through erythropoietin), activate vitamin D (for bone health), and maintain the acid-base balance of the blood.
In CKD, the gradual loss of functioning nephrons (the individual filtering and processing units that make up each kidney) reduces the kidneys' ability to perform all these functions. As nephrons are lost, the remaining nephrons compensate by filtering at higher rates a phenomenon called hyperfiltration which sustains adequate function but at the cost of progressive stress on the surviving nephrons. This hyperfiltration itself accelerates further loss, creating a self-reinforcing cycle of nephron loss that explains why CKD, once established beyond a certain point, tends to progress even without the original cause continuing to operate.
The five stages of CKD — and what each means
CKD is staged using the estimated Glomerular Filtration Rate (eGFR) — a calculation from the serum creatinine level, age, and sex that estimates the kidney's filtration rate in ml per minute per 1.73m² of body surface area. Normal eGFR in a young adult is 90 to 120 ml/min/1.73m².
Stage 1 · eGFR ≥ 90
Clinical situation: Kidney function is normal or near-normal but there is evidence of kidney damage (protein in urine, blood in urine, structural abnormality on imaging). Stage 1 CKD is often detected only on routine testing. Action at KIMS: Identify and treat the underlying cause · control blood pressure and blood sugar · monitor eGFR and urine protein annually.
Stage 2 · eGFR 60–89
Clinical situation: Mildly reduced still largely asymptomatic. The most important stage for lifestyle and medication intervention to slow progression. Action at KIMS: Intensify BP control · SGLT2 inhibitor in diabetics · restrict sodium and protein (moderate) · annual nephrology review.
Stage 3 · eGFR 30–59
Clinical situation: Moderately reduced. Anaemia, bone disease, and hypertension complications begin to emerge. Symptoms may start fatigue, mild ankle swelling. Action at KIMS: Nephrology review every 6 months · manage anaemia (erythropoietin if needed) · phosphate and vitamin D management · fistula evaluation begins at lower end of Stage 3 if progression trajectory warrants.
Stage 4 · eGFR 15–29
Clinical situation: Severely reduced. Symptoms become more prominent. This is the critical stage for transplant and dialysis planning. Action at KIMS: Mandatory nephrology review every 3 months · AV fistula creation planned and typically performed at Stage 4 (3–6 months before anticipated dialysis need) · transplant evaluation initiated · education about dialysis modalities · dietitian involvement for protein and potassium management.
Stage 5 · eGFR < 15
Clinical situation: Kidney failure / End-Stage Renal Disease (ESRD). The kidneys can no longer sustain life without renal replacement therapy. Action at KIMS: Initiation of haemodialysis, peritoneal dialysis, or kidney transplant (ideally pre-emptive transplant without dialysis first). Aarogyasri, CGHS, EHS coverage initiated for dialysis.
The most important clinical action in CKD management is creating an AV fistula at Stage 4 — 3 to 6 months before dialysis is anticipated. A patient who starts dialysis with a mature fistula already in place avoids weeks or months on a central venous catheter, which carries 10 to 15 times higher infection risk. Most CKD patients are never told this until they are already in kidney failure at KIMS, fistula planning begins as a routine part of Stage 4 management.
What causes CKD?
In Hyderabad and across Telangana, the two most common causes of CKD are diabetes mellitus (diabetic nephropathy) and hypertension (hypertensive nephrosclerosis) accounting for more than half of all CKD cases seen at KIMS. Understanding the cause is essential, because:
Diabetic nephropathy
Develops after 5 to 15 years of poorly controlled diabetes. The mechanism is glucose-mediated glomerular injury. Detection: microalbuminuria (tiny amounts of protein in urine, detectable before creatinine rises). Prevention: HbA1c below 7%, blood pressure below 130/80, SGLT2 inhibitors (empagliflozin, dapagliflozin now proven to slow diabetic nephropathy independently of blood sugar control), ACE inhibitors or ARBs to reduce proteinuria.
Hypertensive nephrosclerosis
High blood pressure causes progressive damage to the small vessels of the kidney. Blood pressure above 140/90 sustained over years narrows and hardens glomerular arterioles. Detection: mildly elevated creatinine, trace proteinuria. Prevention and management: strict blood pressure control below 130/80 (ACE inhibitor or ARB as first choice they have specific kidney-protective effects beyond blood pressure reduction alone).
Glomerulonephritis
Immune-mediated inflammation of the glomeruli, including IgA nephropathy (the most common), membranous nephropathy, FSGS, and lupus nephritis. Diagnosis requires kidney biopsy. Treatment depends on the specific histological subtype.
Chronic obstruction
Longstanding BPH, ureteric stricture, or other causes of urinary tract obstruction cause back-pressure damage to the kidney (obstructive nephropathy). Relieving the obstruction (TURP, HoLEP, or ureteric stent) stops progression but may not fully reverse established damage.
Recurrent kidney infection / pyelonephritis
Repeated upper urinary tract infections scar the kidney. Common in women with structural urinary tract abnormalities or reflux nephropathy.
Inherited
Polycystic Kidney Disease (PKD), Alport syndrome, and other genetic conditions.
Symptoms of CKD — and why they appear so late
Because the kidneys have enormous reserve capacity and the remaining nephrons compensate for lost ones, CKD typically produces no symptoms until eGFR falls below approximately 25 to 30 ml/min. By this point, 70 to 75% of kidney function has already been lost. The symptoms that eventually emerge reflect the accumulated failure of all kidney functions:
Fatigue — often the earliest and most prominent symptom. Results from anaemia (reduced erythropoietin production) and uraemic toxin accumulation affecting cellular energy metabolism.
Ankle and leg swelling — fluid retention from reduced sodium and water excretion.
Breathlessness — in advanced CKD, fluid accumulates in the lungs (pulmonary oedema). Can be mistaken for cardiac or respiratory disease.
Reduced urine output — in advanced CKD, the kidneys lose the ability to concentrate urine and regulate output. Oliguria (very low output) signals severe kidney failure.
Nausea and loss of appetite — uraemia (accumulation of urea and other waste products) has a direct toxic effect on the gastrointestinal tract and the brain.
Itching — accumulation of phosphate and other uraemic toxins causes severe, difficult-to-treat pruritus.
Bone pain and fractures — renal osteodystrophy from abnormal phosphate, calcium, and vitamin D metabolism weakens bones.
Cognitive symptoms — uraemic encephalopathy in severe CKD produces confusion, difficulty concentrating, and in extreme cases seizures.
Most of these symptoms are reversible or manageable with appropriate CKD care or, in advanced disease, with dialysis or transplant. Starting treatment before symptoms appear, at Stage 3 or Stage 4, is always better than starting at the onset of symptomatic kidney failure.
CKD management at KIMS — slowing progression at every stage
CKD management at KIMS is built around four evidence-based pillars that, applied consistently from early stages, have the best evidence for slowing progression and reducing complications:
Blood pressure control
Target blood pressure in CKD is below 130/80 mmHg for most patients, below 125/75 for patients with significant proteinuria. ACE inhibitors (ramipril, enalapril) or ARBs (losartan, olmesartan) are the first choice they reduce proteinuria and slow glomerular injury independently of blood pressure reduction. The KIMS nephrology team monitors blood pressure at every visit and adjusts medications aggressively to target.
SGLT2 inhibitors
The landmark DAPA-CKD and CREDENCE trials demonstrated that SGLT2 inhibitors (dapagliflozin, empagliflozin) significantly reduce the rate of CKD progression and kidney failure events in patients with CKD both in diabetics and non-diabetics. These medications are now standard of care for CKD with proteinuria. KIMS integrates SGLT2 inhibitor prescription into the routine CKD management protocol for eligible patients.
Dietary management
A low-sodium diet reduces blood pressure and fluid retention. Protein restriction (0.6 to 0.8g/kg/day) in advanced CKD reduces uraemic toxin production. Potassium restriction becomes important in Stage 4 and 5 as kidney loses ability to excrete potassium. Phosphate restriction (limiting dairy, nuts, processed foods) reduces secondary hyperparathyroidism, bone disease. KIMS renal dietitian provides guidance at Stage 3 and 4 consultations.
Anaemia management
Erythropoietin stimulating agents (ESAs — darbepoetin, EPO) are used when haemoglobin falls below 10g/dl from renal causes. Iron stores must be optimised before starting ESAs iron deficiency reduces their effectiveness. Target haemoglobin on ESA therapy is 10 to 12g/dl higher targets are associated with increased cardiovascular risk.
When to see a nephrologist for CKD
Primary care physicians and diabetologists appropriately manage early CKD. But there are specific situations where specialist nephrology review at KIMS is strongly recommended — and where delayed referral consistently leads to worse outcomes:
eGFR below 45 (Stage 3b)
At this level, management complexity increases significantly and specialist input optimises the treatment strategy.
Rapid decline
A fall of 5 ml/min/1.73m² or more in eGFR within 12 months indicates accelerating progression requiring specialist evaluation of the cause and management adjustment.
Significant proteinuria
Protein/creatinine ratio above 300mg/g indicates significant glomerular disease requiring kidney biopsy consideration.
Unexplained CKD
No clear diagnosis of diabetic nephropathy or hypertensive nephrosclerosis despite investigation. Biopsy may identify a treatable glomerular disease.
Refractory anaemia
Haemoglobin below 10g/dl not responding to iron supplementation.
Uncontrolled blood pressure
Blood pressure remaining high despite being on multiple agents.
eGFR below 30 (Stage 4)
Mandatory nephrology referral for transplant and dialysis planning, AV fistula creation timing, and intensified complication management.
If you have diabetes or hypertension, ask your doctor to check your eGFR and urine albumin-to-creatinine ratio at least once a year. These two tests together identify CKD in its earliest, most treatable stages and both are simple blood and urine tests available at any laboratory. At KIMS, these tests are included in every routine diabetic and hypertensive patient review.
Frequently Asked Questions — CKD
CKD cannot be reversed — the kidney tissue already lost does not regenerate. However, progression can be significantly slowed, and in some cases of early CKD caused by a reversible condition (such as obstructive nephropathy from BPH, or glomerulonephritis treated with immunosuppression), stabilisation or modest improvement in eGFR is possible. The goal of CKD management is to preserve as much function as possible for as long as possible — delaying the need for dialysis or transplant by years or even decades in some patients. At KIMS, the combination of blood pressure control, SGLT2 inhibitors, dietary management, and complication treatment achieves this goal in most Stage 1 to Stage 3 patients.
Acute Kidney Injury (AKI) is a sudden, rapid decline in kidney function — over hours to days — caused by a specific acute event such as sepsis, dehydration, a nephrotoxic drug, or urinary obstruction. AKI is potentially reversible: if the underlying cause is identified and treated quickly, kidney function often recovers — sometimes completely. CKD, by contrast, is a chronic, progressive loss of function over months to years. AKI and CKD can coexist: a patient with pre-existing CKD is more susceptible to AKI episodes, and repeated AKI episodes accelerate CKD progression. A patient who has had an AKI episode should have kidney function checked at 3 months to determine whether recovery is complete or whether CKD has developed.
No — most CKD patients never reach kidney failure requiring dialysis. Studies show that the majority of patients with CKD Stages 1 to 3 — particularly those managed well for blood pressure and diabetes — die of cardiovascular disease before their kidneys fail, because CKD at moderate stages is a powerful risk factor for heart attack and stroke. Optimising CKD management simultaneously reduces both the cardiovascular risk and the risk of progression to kidney failure. For patients who do progress — particularly those with rapid eGFR decline or significant proteinuria — kidney failure requiring dialysis or transplant may eventually develop. But even then, transplant provides dramatically better outcomes than long-term dialysis.
Dietary management in CKD is specific to the stage and the underlying cause, and should be guided by the KIMS renal dietitian based on blood test results rather than generic internet advice. However, general principles: high potassium foods (bananas, tomatoes, oranges, potatoes, legumes) should be limited from Stage 3b onwards as the kidney loses the ability to excrete potassium — dangerous hyperkalaemia can cause cardiac arrest. High phosphate foods (dairy, nuts, whole grains, processed foods, dark fizzy drinks) should be restricted in Stage 3 and above to prevent bone disease and vascular calcification. Sodium restriction (limiting salt and processed/packaged foods) reduces blood pressure and fluid retention at all stages. High protein diets (more than 1.2g/kg/day) should be avoided in Stage 3 and above as they increase uraemic toxin production.
At CKD Stage 4 — typically when eGFR falls below 20 to 25 ml/min and dialysis is anticipated within the next 6 to 12 months. A fistula takes 4 to 8 weeks to mature before it can be used for dialysis. Creating it at Stage 4 ensures it is ready when dialysis is needed — avoiding the alternative of starting dialysis through a central venous catheter in the neck, which carries 10 to 15 times higher infection risk. At KIMS, every CKD patient with eGFR below 20 is referred for fistula evaluation as a routine part of Stage 4 management — not when kidney failure arrives.
Specific treatments for CKD complications are covered under Aarogyasri (PMJAY) at KIMS — including haemodialysis sessions, kidney transplant, AV fistula creation, and some investigations. Routine CKD outpatient management (consultations, blood tests, medications) is covered under outpatient provisions of Aarogyasri at empanelled hospitals. KIMS is empanelled under Aarogyasri, CGHS, and EHS — the KIMS billing desk can confirm coverage for specific procedures and medications at the consultation.
KIMS Secunderabad — the nephrology team at KIMS includes senior specialists (Dr. V. S. Reddy, Dr. E. Ravi) with 15 to 20+ years of CKD and transplant experience, and subspecialty expertise across glomerular disease (Dr. Aswini Dutt T), critical care nephrology (Dr. E. Ravi), and women's nephrology (Dr. Susmitha Chandragiri). The same nephrologist manages CKD from the earliest stages through to dialysis and transplant — providing the continuity of care that complex kidney disease requires. NABH and NABL accredited. 1,500+ kidney transplants performed. Call 040 - 44885000 to book a CKD consultation.