Definition and Diagnostic Criteria
Chronic kidney disease (CKD) is a persistent decline in renal function lasting for at least 3 months. The term CKD is broader than "chronic renal failure" and encompasses it as one of its stages.
Key diagnostic criteria:
- Decrease in glomerular filtration rate (GFR) below 60 mL/min/1.73 m² persisting for ≥3 months;
- Albuminuria — increased urinary albumin excretion; evaluated either by 24-hour urinary protein loss or by the albumin-to-creatinine ratio in a spot urine sample;
- Structural or functional renal abnormalities detected by ultrasound;
- Urinary sediment abnormalities: hematuria, cylindruria.
To calculate GFR based on serum creatinine levels, the CKD-EPI formula is used. Creatinine is produced in muscles from the breakdown of creatine and creatine phosphate and is almost entirely excreted by the kidneys, allowing glomerular filtration to be assessed via its concentration.
Main Causes of CKD
About 45% of CKD cases are caused by diabetic nephropathy. Chronic hyperglycemia leads to non-enzymatic protein glycation, endothelial damage, and preferential thickening of the glomerular efferent arteriole. Hydrostatic pressure in the glomerular capillaries and the effective filtration pressure increase, causing hyperfiltration and gradual destruction of nephrons.
Hypertensive nephropathy is characterized by thickening of the afferent arteriole. Reduced renal blood flow activates the juxtaglomerular apparatus and the RAAS: angiotensin II causes vasoconstriction, and aldosterone enhances sodium and water reabsorption. Parenchymal ischemia develops, establishing a vicious cycle with the progression of arterial hypertension.
The third major group is glomerulonephritis, in which immune complexes damage the glomerular basement membrane. In all variants, mesangial cells play a key role in progression: they increase extracellular matrix synthesis, leading to glomerulosclerosis and nephron loss.
Complications of CKD
Hypervolemia is a consequence of sodium and water retention; it manifests as leg edema, pulmonary edema, and maintains secondary arterial hypertension.
Metabolic acidosis occurs due to impaired proton secretion and bicarbonate reabsorption. The decrease in pH is accompanied by potassium efflux from cells in exchange for protons, resulting in hyperkalemia. On ECG: tall peaked T waves, prolonged PR interval, disappearance of the P wave, widened QRS complex.
Mineral and bone disorders and secondary hyperparathyroidism. Phosphate retention and decreased synthesis of α-1-hydroxylase reduce the production of active vitamin D (calcitriol), leading to decreased intestinal calcium absorption. Hypocalcemia and hyperphosphatemia stimulate the parathyroid glands, increasing parathyroid hormone (PTH) secretion and activating osteoclasts — resulting in osteoporosis and calciphylaxis (deposition of calcium salts in the vascular intima with tissue ischemia and trophic ulcers). With prolonged disease, the parathyroid glands acquire autonomy, forming tertiary hyperparathyroidism with hypercalcemia.
Anemia of chronic disease is caused by three mechanisms: decreased erythropoietin synthesis by peritubular cells, elevated hepcidin levels in chronic inflammation (ferroportin blockade and impaired iron absorption), and shortened erythrocyte lifespan in the uremic environment.
Uremia, caused by the accumulation of urea and nitrogenous waste products, leads to uremic encephalopathy with asterixis, uremic pericarditis (ECG shows ST elevation and PR depression), and platelet dysfunction with a hemorrhagic diathesis.
Dyslipidemia develops due to compensatory hepatic synthesis of low-density and very low-density lipoproteins in response to urinary albumin loss.
Staging and Diagnostic Principles
CKD stages are determined by the GFR level (C1–C5) and albuminuria category (A1–A3) according to the KDIGO classification. End-stage renal disease (C5) corresponds to chronic renal failure.
The minimum diagnostic workup includes:
- serum creatinine with GFR calculation;
- urinalysis, albuminuria (24-hour or albumin-to-creatinine ratio);
- serum electrolytes — potassium, sodium, calcium, phosphorus;
- acid-base status parameters, bicarbonate level;
- hemoglobin, ferritin, transferrin saturation;
- parathyroid hormone, 25(OH)-vitamin D;
- lipid profile;
- renal ultrasound, ECG.
Management of Complications
- Metabolic acidosis: administration of sodium bicarbonate, especially when pH < 7.2.
- Hyperkalemia: potassium-restricted diet, loop diuretics (furosemide), potassium-binding resins; in emergency situations — insulin with glucose, calcium gluconate, ECG monitoring.
- Hypervolemia: dietary salt restriction, loop diuretics, daily weighing.
- Arterial hypertension: ACE inhibitors or angiotensin II receptor blockers — RAAS blockade with nephroprotective effects.
- Anemia: iron replenishment (preferably intravenous due to impaired absorption), erythropoiesis-stimulating agents if anemia persists; target hemoglobin 100–120 g/L.
- Mineral and bone disorders: phosphorus-restricted diet, phosphate binders, calcitriol, calcimimetics; parathyroidectomy if ineffective.
- Dyslipidemia: statins.
Renal Replacement Therapy
Indications for dialysis are remembered by the mnemonic "AEIOU": acidosis, electrolyte abnormalities, intoxications, volume overload, uremia (encephalopathy, pericarditis, bleeding diathesis).
Hemodialysis is performed via a vascular access — an arteriovenous fistula (matures in 1.5–2 months), a synthetic shunt graft, or a central venous catheter for urgent needs. The procedure is carried out 3 times a week for 3–4 hours in a dialysis center, based on the principles of diffusion and convection.
Peritoneal dialysis uses the peritoneum as a natural semipermeable membrane: dialysate is infused into the abdominal cavity via a catheter and exchanged according to a schedule. The method can be performed at home; the main complication is peritonitis.
Kidney transplantation is the optimal replacement therapy method in the absence of contraindications. It requires immunological matching and lifelong immunosuppression. Following transplantation, monitoring of GFR, blood pressure, hemoglobin, ferritin, calcium, vitamin D, ECG, and graft ultrasound is mandatory.
Key points
- CKD is diagnosed when GFR < 60 mL/min/1.73 m² and/or signs of renal damage persist for ≥3 months.
- Three leading causes: diabetic nephropathy, hypertensive nephropathy, glomerulonephritis.
- The universal mechanism of progression is mesangial glomerulosclerosis and nephron loss.
- Main complications: hypervolemia, acidosis, hyperkalemia, secondary and tertiary hyperparathyroidism, anemia, uremia, dyslipidemia.
- Hyperkalemia on ECG: tall T waves, prolonged PR, widened QRS, absent P.
- Nephroprotection is based on RAAS blockade with ACE inhibitors or ARBs and glycemic control.
- Anemia is corrected with iron preparations and erythropoiesis-stimulating agents targeting an Hb of 100–120 g/L.
- Indications for dialysis: acidosis, electrolyte abnormalities, intoxications, volume overload, uremic complications.