Acute renal failure

Impact of hypertension on the development of renal failure

The development of renal failure (both acute and chronic) is closely linked to the stage and clinical form of hypertension. The direct mechanisms leading to death vary depending on the clinical variant of the pathology:

• In the malignant form of hypertension, rapid target organ damage causes acute or chronic renal failure, which becomes the main cause of patient death.
• Acute progression of the disease, manifesting as hypertensive crises and vascular catastrophes, can also provoke acute renal failure. In addition, in this phase, death may result from myocardial infarction, acute cerebrovascular accident (stroke), rupture of a dissecting aortic aneurysm, or massive hemorrhages into internal organs, including brain tissue.
• For the benign form with a long anamnesis, a gradual development of chronic renal or heart failure is more characteristic.
• The formation of arteriolosclerotic nephrosclerosis predictably culminates in chronic renal dysfunction and progressive azotemic uremia.

Pathogenesis of malignant nephrosclerosis

One of the most severe renal complications is malignant nephrosclerosis. This form of pathology is inextricably linked to the accelerated (malignant) phase of arterial hypertension, which may be of nephrogenic or renovascular origin.

The pathogenesis is based on pronounced ischemia of the renal parenchyma, which acts as a potent stimulus for the hyperactivation of the renin-angiotensin-aldosterone system (RAAS). The cascade of reactions develops according to the following scenario:

1. Critical hyperreninemia occurs, accompanied by high concentrations of angiotensin and aldosterone.
2. These biologically active substances provoke generalized blood vessel spasm.
3. A sharp, uncontrolled spike in blood pressure takes place.
4. Extreme hemodynamic load combined with ischemia leads to necrosis of renal vessels and other internal organs, which can clinically manifest as acute renal failure.

Extrarenal manifestations of uremia

Uremia developing in severe forms of renal failure and nephrosclerosis against the background of hypertension triggers a number of systemic pathological processes. These extrarenal manifestations significantly contribute to thanatogenesis and affect most body systems:

• Cardiovascular system: toxin accumulation causes uremic pericarditis. Concurrently, left ventricular hypertrophy develops as a consequence of prolonged arterial hypertension.
• Gastrointestinal tract: characteristic development of uremic gastroenteritis (up to fibrinous-hemorrhagic gastroenterocolitis).
• Respiratory system: toxic damage to lung tissue manifests as uremic pneumonitis, based on specific diffuse alveolar damage.
• Bone and endocrine system: impaired mineral metabolism leads to secondary hyperparathyroidism. As a consequence of the latter, calcium salts are deposited in tissues (nephrocalcinosis) and renal osteodystrophy develops.
• Central nervous system: azotemic intoxication inevitably leads to damage to neural structures with the formation of uremic encephalopathy.

Glomerulopathies and the rate of renal function loss

The outcome of most glomerular diseases is the formation of a secondary shrunken kidney (nephrosclerosis) through a stage of chronic inflammation. However, the dynamics of this process directly depend on the morphological variant of the disease:

• Rapidly progressive glomerulonephritis: characterized by an extremely aggressive course. If the patient successfully survives the acute phase, nephrosclerosis develops in a very short time.
• Focal segmental glomerulosclerosis: characterized by a rapid increase in symptoms of renal failure.
• Membranous nephropathy, mesangiocapillary glomerulonephritis, and IgA nephropathy: characterized by slow, gradual progression to terminal stages.
• Latent forms: proceed asymptomatically. Often, the primary variant of glomerulonephritis cannot be established, and the disease is diagnosed already at the stage of outcome in uremia.

The direct causes of death for such patients are uremia itself with its toxic effects, cardiovascular decompensation (against the background of nephrogenic hypertension and myocardial hypertrophy), massive intracerebral hemorrhages, as well as intercurrent infections joining due to secondary immunodeficiency.

Class and exam questions

What else to study on this topic

• Mechanisms of secondary shrunken kidney formation in various morphological types of glomerulonephritis.
• Pathogenesis of nephrotic syndrome and associated metabolic disorders.
• Thanatogenesis in acute myocardial infarction: cardiogenic pulmonary edema and fatal arrhythmias.
• Morphological picture of diffuse alveolar damage in uremic pneumonitis.
• The relationship between uremia and the formation of secondary immunodeficiency with the development of intercurrent infections.

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