25 topics with concise breakdowns: definitions, key facts, and class questions.
This section focuses on morphological changes in pathologies of the urinary system. We will analyze how glomeruli, tubules, the interstitium, and the urinary tract are damaged — from the initial microscopic shifts to end-stage renal disease (nephrosclerosis).
The materials cover all key nosologies: a broad group of glomerulopathies (ranging from minimal change disease and acute glomerulonephritis to IgA nephropathy), renal involvement in systemic processes (diabetic nephropathy, amyloidosis, myeloma kidney, Alport syndrome), as well as acute tubular necrosis and tubulointerstitial nephritis, including chronic pyelonephritis. Frequently encountered urological pathologies are reviewed separately: urolithiasis, cystitis, and tumors of the kidney and urinary bladder.
In seminars and exams, the morphology and pathogenesis of glomerulonephritides are tested most rigorously (especially focal segmental glomerulosclerosis and membranous nephropathy). Pay special attention to the markers of rapidly progressive glomerulonephritis (" crescents"), as well as the macroscopic and microscopic picture of the kidneys in diabetes and amyloidosis — these are classic exam tasks.
Why do all structures of the organ ultimately suffer in chronic kidney disease?
This occurs due to the close pathogenetic interconnection of structures. For example, the destruction of glomeruli disrupts peritubular blood flow, while tubular destruction increases intraglomerular pressure, leading to their atrophy. Ultimately, total damage develops.
What is the difference between immune complex fluorescence in circulating versus in situ mechanisms?
When circulating complexes are deposited, granular fluorescence is observed under the microscope, whereas upon in situ complex formation (directly on the basement membrane), linear fluorescence is observed.
What is the primary mechanism of development of acute glomerulonephritis?
The disease is immunologically mediated and develops via an immune-complex mechanism, as confirmed by the detection of granular immune deposits in the glomeruli.
What is the main morphological marker of rapidly progressive glomerulonephritis?
The main morphological marker is the formation of epithelial crescents in the majority of renal glomeruli.
Where exactly are immune deposits located in membranous nephropathy?
The deposits are located along the epithelial side of the basement membrane, i.e., subepithelially, directly beneath the podocytes.
Why are lipids found in the tubules in minimal change disease?
Due to damage to the glomerular filtration barrier, lipoproteins enter the urine. The proximal tubules actively reabsorb them, leading to lipid accumulation in epithelial cells.
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