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Acquired cystic disease of kidney in chronic dialysis patients
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Acquired cystic disease of the kidney (ACDK) in patients with chronic renal failure and hemodialysis is distinct from congenital adult polycystic kidney disease (CAPKD). ACDK kidneys are smaller and feature cysts replacing significant renal parenchyma.
Area of Science:
- Nephrology
- Pathology
- Urology
Background:
- Acquired cystic disease of the kidney (ACDK) is a condition observed in patients with chronic renal failure undergoing hemodialysis.
- Distinguishing ACDK from congenital adult polycystic kidney disease (CAPKD) is crucial for accurate diagnosis and management.
Purpose of the Study:
- To describe the clinical and morphological features of acquired cystic disease of the kidney (ACDK) in patients with chronic renal failure.
- To highlight key differentiating factors between ACDK and congenital adult polycystic kidney disease (CAPKD).
Main Methods:
- Case series describing eight patients with ACDK.
- Clinical data collection including etiology of renal failure and complications.
- Morphological examination of kidneys, including weight and cyst prevalence.
- Nephron dissection to establish cyst-tubule continuity.
Main Results:
- Eight cases of ACDK in patients with chronic renal failure and hemodialysis were identified.
- Glomerulonephritis and pyelonephritis were the primary causes of renal failure.
- Massive hemorrhage occurred in some cases, necessitating nephrectomies.
- Kidney weights were below 280 Gm., distinguishing ACDK from CAPKD.
- Cysts replaced 40-80% of renal parenchyma, with continuity to tubules observed.
Conclusions:
- ACDK presents distinct morphological characteristics, notably smaller kidney size, compared to CAPKD.
- The presence of extensive cystic changes and their connection to tubules are key features of ACDK.
- Early recognition of ACDK is important for managing potential complications like hemorrhage.
Abstract:
Eight cases of acquired cystic disease of the kidney (ACDK) associated with chronic renal failure and hemodialysis are described. No patient had a family history or clinical evidence of congenital adult polycystic kidney disease (CAPKD). Glomerulonephritis was the cause of renal failure in 6, and pyelonephritis in 2. Massive renal and perirenal hemorrhage necessitated 3 nephrectomies in 2 patients. Single kidney weights did not exceed 280 Gm., a major feature in the distinction of ACDK from CAPKD. Morphologically, in addition to the usual stigmata of end-stage kidneys, 40 to 80 per cent of the renal parenchyma was replaced by small cysts. Continuity of cysts with tubules was established by nephron dissection.