Abstract
Наведено клінічний випадок з особливостями морфологічної картини гострого гломерулонефриту, що перебігав на фоні попередньо існуючої патології канальцевого апарату нирок — мікрополікістозу некласифікованого. Хворому Х., 20 років, була проведена патогенетична терапія гострого гломерулонефриту глюкокортикоїдами та цитостатиками. Однак, незважаючи на застосовані терапевтичні засоби, симптоми гломерулонефриту продовжували наростати, розвинувся нефротичний синдром, що призвело до критичної втрати білків плазми крові, розладів коагуляції у вигляді ДВЗ-синдрому та подальшого приєднання уремії. Імовірно, резистентність до лікування пов’язана з попередньо існуючою патологією канальців нирок, функція яких була скомпрометована, та, можливо, генетично детермінованою резистентністю до патогенетичної терапії.
Highlights
Acute postinfectious glomerulonephritis (APGN) is a multifactorial immune-related kidneys’ inflammation with initial damage of renal glomeruli with further involvement of all nephron structures into the pathological process
Most cases of APGN related to streptococcal etiology
The pathogenesis of the APGN related to deposition of bacterial antigens with further in situ immune complexes formation and deposition of circulating immune complexes in renal glomeruli
Summary
Acute postinfectious glomerulonephritis (APGN) is a multifactorial immune-related kidneys’ inflammation with initial damage of renal glomeruli with further involvement of all nephron structures into the pathological process. Policystic kidney disease (PCKD) is heterogenous entity comprising various genetically determined lesions characterized by development of cysts in renal parenchyma. Regarding rapid progression of disease, the pathogenetic therapy by glucocorticoids has been performed, but nephrotic syndrome with heavy protein loss were still developing. In presented case histopathologic examination of kidney biopsy shows cystic dilation of cortical and medulary tubules of undefined type. This tubular abnormality has been asymptomatic during patients lifetime and complicated the clinical course and outcome of APGN. The clinical course of APGN in presented case characterized by critical loss of plasma proteins, uremia leading to disseminated intravascular coagulation, vein thrombosis, multiple haemorrhages on skin and mucous membranes. Inexorable decline of renal function can be related to renal tubules abnormality – polycystic kidney disease of undefined type
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