175. Urolithiasis: etiology, chemical composition of stones, mechanism of stone formation. Macro- and microscopic changes in the kidneys, complications, outcomes.

Urolithiasis (nephrolithiasis) is a disease in which stones of different sizes, structures and chemical composition are formed in the renal cups, pelvis and ureters: phosphates, urates, oxalates, carbonates. The disease has a chronic course, one or both kidneys are involved in the process.

Etiology:

Of the common factors contributing to nephrolithiasis, hereditary and acquired disorders of calcium, phosphorus, uric acid, oxalic acid metabolism, acidosis, the predominance of carbohydrates and animal proteins in food, the mineral composition of drinking water (endemic nephrolithiasis) and beriberi A. Local factors of stone formation are factors that change the physico—chemical state of urine and thus contribute to salt loss. Inflammation of the urinary tract and urinary stasis play an important role. These factors lead to an increase in the concentration of salts in the urine, a change in the pH and colloidal balance of urine, and the formation of a colloidal (protein) stone base. Of great importance in the development of nephrolithiasis are trophic and motor disorders of the functions of the cups, pelvis, ureters — atony of the pelvis and ureters, circulatory disorders.

The chemical composition of the stones:

The most common types of kidney stones are:

calcium stones (mixed calcium oxalates/phosphates, calcium oxalates, calcium phosphates)

magnesium and ammonium phosphates (struvite stones)

urates (uric acid stones)

The mechanism of stone formation:

The mechanism of stone formation is associated with the inability to completely empty the bladder, stagnation and concentration of residual urine, leading to the loss of salt crystals.

Macro- and microscopic changes:

Changes in nephrolithiasis are extremely diverse and depend on the localization of stones, their size, the duration of the process, and the presence of infection.

A pelvis stone that disrupts the outflow of urine leads to pyeloectasia, and later to hydronephrosis with atrophy of the renal parenchyma; the kidney turns into a thin—walled, urine-filled sac. If the stone is in the calyx, then a violation of the outflow from it leads to the expansion of only the calyx — hydrocalicosis, and only part of the renal parenchyma is subject to atrophy. A stone obstructing the ureter causes an expansion of the pelvis and ureteral lumen above the obturation — hydroureteronephrosis. In this case, inflammation of the ureteral wall occurs — ureteritis, which leads to stricture; sometimes a bedsore forms with perforation of the ureter at the site of its blockage. The addition of infection changes the morphological picture of nephrolithiasis. Infected calculous hydronephrosis (hydroureteronephrosis) becomes pionephrosis (pioureteronephrosis). Infection leads to the development of pyelitis, pyelonephritis, apostematous (pustular) nephritis, and purulent melting of the parenchyma. Inflammation often passes to the perinephrine tissue, causing chronic paranephritis. In such cases, the kidney is immured in a thick capsule of granulation, fatty and fibrous tissues (carapace paranephritis), and sometimes completely replaced by sclerosed fatty tissue (fatty kidney replacement).

The most common complication of urolithiasis is pyelonephritis. Especially dangerous are pyonephrosis and purulent melting of the kidney, which sometimes end in sepsis. Acute renal failure is rare. Prolonged course of urolithiasis, atrophy, fibrous and fatty kidney replacement lead to chronic renal failure.

Outcomes: with a favorable course, spontaneous discharge of the stone occurs, its surgical extraction is possible. Death of patients with nephrolithiasis often occurs from uremia and complications of purulent melting of the kidney.