Chronic Kidney Disease

Genitourinary

Description

Chronic kidney disease is a long-standing, usually irreversible reduction in glomerular filtration rate or evidence of structural kidney injury such as albuminuria, haematuria or imaging abnormalities that persists for at least three months and impairs the kidneys’ ability to excrete nitrogenous waste, balance electrolytes, maintain acid–base homeostasis, regulate blood pressure and perform endocrine functions. KDIGO 2024 continues to classify CKD by cause, G-stage (G1 ≥ 90 to G5 < 15 mL/min/1.73 m²) and A-stage of albuminuria, emphasising that both diminished eGFR and elevated urine albumin independently drive cardiovascular and renal risk.

Symptoms

Early CKD is clinically silent; as filtration falls below 30 mL/min/1.73 m² patients may notice nocturia, fatigue, anorexia, pruritus, muscle cramps, peripheral oedema or refractory hypertension. Advanced disease produces nausea, vomiting, cognitive clouding, restless legs, dyspnoea from pulmonary oedema and pericardial pain from uraemic serositis. Physical findings include pallor of anaemia, sallow discoloration, foamy urine, bilateral pitting oedema, hypertension and asterixis in severe uraemia.

Risk Factors

The leading causes are type 2 diabetes mellitus and long-standing hypertension, followed by glomerulonephritides, obesity, metabolic syndrome, smoking, atherosclerotic renal artery stenosis, recurrent pyelonephritis, obstructive uropathy, systemic autoimmune disease, HIV infection, hepatitis C, chronic analgesic or NSAID use, exposure to heavy metals or herbal aristolochic acid, and heritable disorders such as autosomal dominant polycystic kidney disease or APOL1 high-risk alleles in individuals of African ancestry. Age over sixty, male sex, low birth weight, low socioeconomic status and family history amplify vulnerability.

Diagnosis

Diagnosis relies on at least two abnormal measurements three months apart: estimated GFR < 60 mL/min/1.73 m² calculated from serum creatinine or cystatin C, urine albumin-to-creatinine ratio ≥ 30 mg/g or structural abnormalities on ultrasound. A standard laboratory panel evaluates electrolytes, bicarbonate, calcium, phosphate, parathyroid hormone, lipids, haemoglobin, ferritin and transferrin saturation. Urinalysis with microscopy identifies dysmorphic red cells or casts suggestive of glomerular pathology; renal ultrasound assesses kidney size and obstruction. When cause is unclear, serology for ANA, anti-GBM, complements, hepatitis, HIV, serum and urine electrophoresis or renal biopsy are pursued.

Treatment

Cornerstones are reno-protective pharmacotherapy, risk-factor control and complication management. ACE inhibitors or ARBs are started in all patients with albuminuria or hypertension; dose titration to the maximally tolerated level slows GFR decline. SGLT2 inhibitors such as dapagliflozin and empagliflozin are now guideline-mandated across GFR down to 20 mL/min/1.73 m² because they reduce renal-failure events and cardiovascular death irrespective of diabetes. Finerenone, a non-steroidal mineralocorticoid-receptor antagonist, further lowers albuminuria and composite renal outcomes in diabetic CKD. Strict blood-pressure control (<130/80 mm Hg), individualised glycaemic targets, statin therapy, weight loss, smoking cessation and salt restriction (<2 g sodium) address modifiable drivers. Sodium–bicarbonate treats metabolic acidosis; phosphate binders and active vitamin D analogues mitigate mineral-bone disorder; erythropoiesis-stimulating agents and intravenous iron correct anaemia. Nephrology referral is recommended when eGFR <30, rapid decline ≥5 mL/min/1.73 m²/year, refractory hypertension, haematuria with proteinuria or uncertain aetiology arise. Timely education on dialysis modalities and transplant evaluation prepares patients for kidney-replacement therapy.

Outlook

CKD progression is heterogeneous; average untreated annual GFR loss in diabetic nephropathy is 3–5 mL/min/1.73 m² but can be halved with contemporary therapy. Cardiovascular mortality is up to twenty times that of age-matched controls by stage G5. Implementation of ACEi/ARB, SGLT2 inhibitors and MR antagonists has reduced end-stage kidney-disease incidence by 30 % in recent cohorts. Pre-emptive transplantation offers the best survival, while timely initiation of home dialysis improves quality of life compared with in-centre haemodialysis.

Complications

Worsening hypertension, left-ventricular hypertrophy, heart failure, coronary and peripheral arterial disease, anaemia of chronic disease, metabolic acidosis, secondary hyperparathyroidism, renal osteodystrophy, hyperkalaemia, volume overload, endocrine dysfunction, immune suppression, malnutrition, pruritus, sleep apnoea and progression to end-stage kidney disease necessitating dialysis or transplantation constitute the major sequelae.

Prevention

Primordial prevention rests on obesity avoidance, regular physical activity, healthy dietary patterns, abstention from smoking and moderation of alcohol. Secondary prevention comprises optimal glycaemic and blood-pressure control, universal screening in at-risk groups, prompt treatment of glomerulonephritis and avoidance of nephrotoxins, including NSAIDs, iodinated contrast without prophylaxis and illicit anabolic steroids.

Support

Patients should monitor blood pressure at home, adhere to low-salt, plant-forward meals with adequate but not excessive protein (0.6–0.8 g/kg/day unless contraindicated), engage in 150 minutes of moderate exercise weekly as tolerated, remain up to date on influenza, pneumococcal and hepatitis B vaccination, review all prescriptions and over-the-counter NSAIDs with pharmacists, and keep regular nephrology follow-up. Family members can help with medication schedules, diet preparation and transport to dialysis or clinic appointments.