What is the pathophysiology of hydronephrosis and hydroureter?

Updated: Dec 16, 2020
  • Author: Dennis G Lusaya, MD; Chief Editor: Bradley Fields Schwartz, DO, FACS  more...
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Answer

Hydronephrosis can result from anatomic or functional processes interrupting the flow of urine. This interruption can occur anywhere along the urinary tract from the kidneys to the urethral meatus. The rise in ureteral pressure leads to marked changes in glomerular filtration, tubular function, and renal blood flow. The glomerular filtration rate (GFR) declines significantly within hours following acute obstruction. This significant decline of GFR can persist for weeks after relief of obstruction. In addition, renal tubular ability to transport sodium, potassium, and protons and concentrate and to dilute the urine is severely impaired.

The extent and persistence of these functional insults is directly related to the duration and extent of the obstruction. Brief disruptions are limited to reversible functional disturbance with little associated anatomic changes. More chronic disruptions lead to profound tubular atrophy and permanent nephron loss.

Increased ureteral pressure also results in pyelovenous and pyelolymphatic backflow. Gross changes within the urinary tract similarly depend on the duration, degree, and level of obstruction. Within the intrarenal collecting system, the degree of dilation is limited by surrounding renal parenchyma. However, the extrarenal components can dilate to the point of tortuosity.

To distinguish acute and chronic hydronephrosis, one may consider acute as hydronephrosis that, when corrected, allows full recovery of renal function. Conversely, in chronic hydronephrosis the loss of function is irreversible even with correction of the obstruction. Early experiments with dogs showed that if acute unilateral obstruction is corrected within 2 weeks, full recovery of renal function is possible. However, after 6 weeks of obstruction, function is irreversibly lost.

Grossly, an acutely hydronephrotic system can be associated with little anatomic disturbance to renal parenchyma. On the other hand, a chronically dilated system may be associated with compression of the papillae, thinning of the parenchyma around the calyces, and coalescence of the septa between calyces. Eventually, cortical atrophy progresses to the point at which only a thin rim of parenchyma is present. Microscopic changes consist of dilation of the tubular lumen and flattening of the tubular epithelium. Fibrotic changes and increased collagen deposition are observed in the peritubular interstitium.


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