Chronic renal failure

Causes and mechanisms of development

Etiological factors are traditionally divided into three groups depending on the localization of the problem:

• Prerenal — associated with impaired blood supply to the kidney or venous outflow.
• Renal — caused by direct damage to the parenchyma.
• Postrenal — caused by obstructions to normal urine outflow.

The boundaries between groups often blur. A prime example is ischemic nephropathy. It is based on both a macrovascular prerenal factor (renal artery stenosis due to atherosclerosis) and a renal factor (occlusion of intrarenal vessels by cholesterol crystals). Such pathology is frequently triggered by invasive interventions in coronary artery disease.

The earliest functional impairment in CRF is the loss of the ability to concentrate urine. The patient begins to excrete large volumes of fluid (polyuria), especially at night (nocturia). Urinalysis reveals isosthenuria — the specific gravity of urine remains fixed at 1.010–1.012, which corresponds to the density of the primary protein-free plasma filtrate.

Stages of CRF by filtration rate

The classification is based on GFR values and reflects the increasing clinical symptoms:

1. Mild degree (GFR 30–50 mL/min). The patient may feel healthy; latent laboratory shifts predominate.
2. Moderate degree (GFR 10–30 mL/min). Systemic disorders are triggered: arterial hypertension, anemic syndrome, and bone damage (osteodystrophy) appear.
3. Severe degree (GFR 5–10 mL/min). Pronounced intoxication develops — nausea, loss of appetite (anorexia), and excruciating pruritus.
4. Terminal degree (GFR less than 5 mL/min). The stage of uremia, when all kidney functions fail, including endocrine functions. Life-threatening conditions occur: pulmonary edema, pericarditis, and uremic coma. Drug therapy is powerless at this stage — only chronic dialysis or kidney transplantation can save the patient.

Clinical presentation and uremia

As kidney tissue is destroyed, polyuria is replaced by a sharp drop in diuresis — oliguria. Neurological symptoms increase: from initial apathy and weakness to convulsions and coma with noisy Kussmaul acidotic breathing.

A prominent dyspeptic syndrome develops: vomiting, hiccups, diarrhea, and a complete aversion to food. The skin becomes dry, with scratch marks. A persistent odor of urine or ammonia can be detected from the mouth, and the tongue becomes dry and brown.

A most characteristic sign of the disease is anemia (E.M. Tareev's historical term — "Bright's disease anemia"). It occurs due to toxic bone marrow depression, accelerated hemolysis, and the cessation of erythropoietin synthesis in the sclerotic kidney. Due to the accumulation of urinary pigments (urochromes), the pale skin acquires a specific greenish hue.

The terminal phase is accompanied by systemic catastrophes:

• Cardiovascular: malignant hypertension and severe arrhythmias against the background of potassium surges.
• Bone and mineral: disruption of calcium, phosphorus, and vitamin D metabolism leads to secondary hyperparathyroidism and osteomalacia.
• Polyserositis: development of pleurisy and pericarditis. The transition of fibrinous pericarditis to exudative causes shortness of breath and cardiac compression.

Laboratory and instrumental diagnostics

Biochemical blood analysis registers an increase in creatinine, ammonia, phosphates, and alkaline phosphatase, as well as an increase in atherogenic lipids (a risk factor for CAD). A complete blood count shows normochromic normocytic anemia, lymphopenia, and thrombocytopenia (manifested by bleeding). Notably, the severity of proteinuria and cylindruria in the urine often decreases in the late stages.

To assess the rate of CRF progression, a graphical method is used: plotting the curve of the reciprocal of serum creatinine. The steeper the slope of this line, the faster the kidneys are failing.

Instrumental investigation of causes includes:

• Ultrasound: baseline screening for calculi, obstructions, polycystic kidney disease, and the "shrunken kidney" sign.
• Arteriography: indicated when renal artery stenosis is suspected.
• Radioisotope renography: universally demonstrates delayed isotope excretion.
• Biopsy: performed exclusively in the earliest stages for precise diagnosis verification.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathogenetic mechanisms of secondary hyperparathyroidism
• Specifics of electrolyte balance disorders: dynamics of potassium, sodium, and magnesium
• Mechanisms of ischemic nephropathy and cholesterol crystal embolization
• Uremic encephalopathy: clinical presentation and pathogenesis

Other topics in the "Urinary System" section

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