Hydronephrosis and Hydroureter
Hydronephrosis and hydroureter are common clinical conditions encountered not only by urologists but also by emergency medicine specialists and primary care physicians. Hydronephrosis is defined as distention of the renal calyces and pelvis with urine as a result of obstruction of the outflow of urine distal to the renal pelvis. Analogously, hydroureter is defined as a dilation of the ureter.
The presence of hydronephrosis or hydroureter can be physiologic or pathologic. It may be acute or chronic, unilateral or bilateral. It can be secondary to obstruction of the urinary tract, but it can also be present even without obstruction.
Obstructive uropathy refers to the functional or anatomic obstruction of urinary flow at any level of the urinary tract. Obstructive nephropathy is present when the obstruction causes functional or anatomic renal damage. Rarely, obstructive nephropathy may occur in the absence of hydronephrosis.  Thus, the terms hydronephrosis and obstruction should not be used interchangeably.
The etiology and presentation of hydronephrosis and/or hydroureter in adults differ from that in neonates and children. Anatomic abnormalities (including urethral valves or stricture, and stenosis at the ureterovesical or ureteropelvic junction) account for the majority of cases in children. In comparison, calculi are most common in young adults, while prostatic hypertrophy or carcinoma, retroperitoneal or pelvic neoplasms, and calculi are the primary causes in older patients. [2, 3]
Hydronephrosis or hydroureter is a normal finding in pregnant women. The renal pelvises and caliceal systems may be dilated as a result of progesterone effects and mechanical compression of the ureters at the pelvic brim. Dilatation of the ureters and renal pelvis is more prominent on the right side than the left side and is seen in up to 80% of pregnant women.  These changes can be visualized on ultrasound examination by the second trimester, and they may not resolve until 6-12 weeks post partum.
For discussion of fetal hydronephrosis, see Antenatal Hydronephrosis.
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.
An autopsy series of 59,064 subjects ranging in age from neonates to geriatric persons reported hydronephrosis in 3.1%.  In this series, differences based on sex did not become apparent until age 20 years. At age 20-60 years, hydronephrosis was more common in women, possibly because of pregnancy and gynecologic malignancy. In men, prostatic diseases were indicated as the cause of the rise in prevalence after age 60 years. Autopsy studies also indicate that hydronephrosis is present in 2-2.5% of children.  The prevalence is slightly higher in boys, most of whom in the study were younger than 1 year.
These occurrence rates likely underestimate the prevalence because conditions such as temporary obstruction due to prior pregnancy or calculi were not included.
In a study that included 112 patients who underwent percutaneous nephrolithotomy, renal ultrasonography performed 4 – 6 weeks after stent removal, clinically silent hydronephrosis was identified in 16%. the hydronephrosis resolved spontaneously in 50% of cases, with a mean time to resolution of 6.3 months. 
Long-standing hydronephrosis may be associated with obstructive nephropathy and renal failure. Patients with complete or severe partial bilateral obstruction also may develop acute or chronic renal failure. In the latter setting, the patient is often asymptomatic and the urinalysis results may be relatively normal or reveal only a few white or red blood cells.  Thus, urinary tract obstruction should be considered in all patients with otherwise unexplained renal insufficiency. The history may be helpful in some cases, possibly revealing symptoms of prostatic enlargement or prior malignancy or renal calculi.
Urinary stasis may result in infection, renal scarring, calculus formation, and sepsis.
Hypertension is occasionally induced by obstruction. The mechanism responsible for the elevation in blood pressure varies with the duration and type of obstruction. What remains unclear, however, is why the factors described below result in hypertension in only a minority of obstructed patients:
Acute, unilateral obstruction can cause hypertension via activation of the renin-angiotensin system; renal vein renin studies lateralize the increase in renin secretion to the obstructed kidney, a finding similar to that in unilateral renal artery stenosis. 
Renin secretion is usually normal in patients with bilateral urinary tract obstruction or obstruction of a solitary functioning kidney.  In this condition, renal failure leading to volume expansion is typically present; the elevation in blood pressure is probably volume mediated and resolves with the diuresis following correction of the obstruction.
The plasma renin activity is also typically normal in chronic unilateral obstruction, and the presence of the contralateral healthy kidney prevents both renal failure and fluid retention.  Furthermore, relief of the obstruction may not correct the hypertension. These observations suggest that the kidney may have incurred some permanent damage and that the elevation in blood pressure is unrelated to the renal disease.
In women, gynecologic cancers and pregnancy are common causes. As such, among younger patients (aged 20-60 y), the frequency of hydronephrosis is higher in women than in men.
In men, obstruction secondary to prostatic hypertrophy and prostate cancer are the major causes of hydronephrosis. Consequently, among older patients (>60 y), the frequency of hydronephrosis is higher in men than in women.
In young adults, calculi are the most common causes of hydroureter and hydronephrosis.
In children and in neonates, the relative frequency of the causes of antenatal hydronephrosis has been determined to be as follows:
Transient – 48%
Ureteropelvic junction obstruction – 11%
Vesicoureteral reflux – 9%
Megaureter – 4%
Multicystic dysplastic kidney – 2%
Ureterocele – 2%
Posterior urethral valves – 1%
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Dennis G Lusaya, MD Associate Professor II, Department of Surgery (Urology), University of Santo Tomas Faculty of Medicine and Surgery; Chairman, Institute of Urology, St Luke’s Medical Center; Head of Urology Unit, Benavides Cancer Institute, University of Santo Tomas Hospital, Philippines
Dennis G Lusaya, MD is a member of the following medical societies: American Urological Association, Philippine College of Surgeons, Philippine Medical Association, Philippine Society of Urological Oncology, Philippine Urological Association
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Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF Clinical Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Research Director, Internal Medicine Training Program, Advocate Christ Medical Center; Consulting Staff, Associates in Nephrology, SC
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Hydronephrosis and Hydroureter
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