Complications of chronic kidney disease

Extrarenal changes in chronic glomerulonephritis

Chronic glomerulonephritis is accompanied not only by local glomerulitis, which evolves into irreversible glomerulosclerosis, but also by severe systemic vascular reactions. A key pathogenetic role here is played by nephrogenic arterial hypertension, which triggers a cascade of extrerenal changes. First of all, compensatory myocardial hypertrophy occurs with predominant thickening of the left ventricular wall.

Significant structural remodeling of arteries and arterioles is observed within the systemic vascular bed. Elastofibrosis develops, and atherosclerotic arterial lesions and arteriolosclerosis progress rapidly. These degenerative processes affect the vessels of the brain, myocardium, retina, and the kidneys themselves. Such changes critically complicate the differential diagnosis between chronic glomerulonephritis and the renal form of essential hypertension, especially at the stage of secondary kidney contraction.

The main causes of death in patients with this pathology are progressive cardiovascular failure and acute cerebral hemorrhage occurring against the background of uncontrolled high blood pressure.

Complications of chronic pyelonephritis and obstructive uropathies

Prolonged persistent bacterial inflammation in the renal tissue (chronic pyelonephritis) inevitably leads to post-infectious scarring and parenchymal sclerosis. This condition is significantly exacerbated by concomitant urological pathology that disrupts urine flow:

• Chronic cystitis: prolonged inflammation of the bladder mucosa causes sclerosis of the vesicoureteral segment. This destroys the closing mechanism and creates secondary vesicoureteral reflux, which sends infected urine back into the kidneys, closing the vicious pathogenetic circle.
• Urolithiasis (nephrolithiasis) and urinary tract obstruction: lead to the combined development of hydronephrosis with atrophy of renal tissue, the formation of purulent abscesses, and agonizing attacks of renal colic.

The final stage of chronic pyelonephritis is pyelonephritic nephrosclerosis (secondary contracted kidney). Like glomerulonephritis, it provokes persistent renoparenchymal arterial hypertension (along with tumors, tuberculosis, and renal trauma) and ends in chronic kidney disease. The most frequent cause of death in such patients is azotemic uremia, often aggravated by cardiovascular catastrophes.

Specific and nonspecific complications of renal pathologies

Severe kidney damage can be accompanied by the development of acute, life-threatening conditions, which are divided into two broad groups.

1. Specific complications:

• Azotemic uremia syndrome — a classic toxic manifestation of end-stage renal disease.
• Shock states: septic (infectious-toxic) shock and acute kidney injury (AKI).
• Hemorrhagic disorders: DIC syndrome, profuse bleeding, and multiple hemorrhages (in brain tissue, pituitary gland, adrenal glands, myocardium).
• Critical edema states: severe pulmonary edema and cerebral edema.
• Acute cardiovascular failure, infectious myocarditis, eclampsia, and mechanical damage (rupture or complete tear of the renal capsule).

2. Nonspecific complications: These include the addition of a secondary bacterial infection against the background of a sharp decline in the body's immune resistance. This group includes pneumonias, purulent otitis media, parotitis, abscesses, various phlegmons, secondary pyelonephritis, and generalized sepsis.

Outcomes and replacement therapy

The prognosis of the disease directly depends on the form and course of the pathological process. While acute glomerulonephritis usually has a favorable outcome and can end in complete recovery of the patient, the subacute and chronic courses are characterized by an unfavorable prognosis.

Chronic glomerulonephritis is recognized as the most frequent cause of end-stage chronic kidney disease. When the native kidneys finally lose their filtration and concentration capacity, conservative drug therapy becomes ineffective. At this stage, the only possible ways to preserve and prolong the patient's life remain apparatus-based chronic hemodialysis and surgical kidney transplantation.

Class and exam questions

What else to study on this topic

• Assessment of glomerular filtration rate (GFR) and the diagnostic role of creatinine
• Mechanisms of diabetic and hypertensive nephropathy development
• Pathogenesis of anemia in chronic kidney disease
• Mineral and bone disorders and secondary hyperparathyroidism in CKD
• Clinical manifestations of uremia and diagnostic criteria for CKD stages
• Indications and methods of renal replacement therapy

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.