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Rats with hereditary hydronephrosis and littermates with normal kidneys were given 1% saline solution instead of drinking water, and renal excretory function, blood pressure, fluid volumes, and plasma renin activity were monitored. A marked increase in blood pressure and positive correlation between blood pressure and plasma volume were found in hydronephrotic rats after five weeks of salt loading, while animals with normal kidneys remained normotensive. No involvement of the renin-angiotensin system could be demonstrated in the observed phenomenon. It is suggested that the impairment of renal excretory function along with the deficiency of antihypertensive reno-medullary factors are responsible for the greater sensitivity of the hydronephrotic rats to the hypertensive stimulus of salt overload.

A study detailing an assay for evaluating hydronephrotic damage is presented. We used nitroblue tetrazolium, which is reduced by intact renal tissue. When marked hydronephrotic damage has occurred little evidence of tetrazolium reducing activity is present. The clinical application has been helpful in determining the extent of damage and the subsequent need for removal of the kidney in question. When the test indicated functioning renal tissue a repair of the obstruction was performed with subsequent improvement in function.

The chronic encapsulated extravasation of urine, most accurately designated as uriniferous perirenal pseudocyst, causes urine to collect within a characteristic complex of radiographic findings including an elliptical soft-tissue mass in the cone of renal fascia. This results in the flank oriented inferomedially with upward and lateral displacement of the lower renal pole, medial displacement of the ureter, obstructive hydronephrosis, and perhaps evidence of extravasation into the mass. Since the clinical recognition of the mass is typically delayed several weeks following the original traumatic episode, prompt radiological diagnosis is essential before irreparable damage to the kidney occurs.

Histological investigation of ureteropelvic junction (UPJ) specimens of 21 patients with congenital hydronephrosis revealed in 7 instances pathological changes, which might be responsible for the obstruction. In 15 cases a significant increase of collagenous tissue within the UPJ, along with a relative deficiency of monocytes was noted. Each of the smooth muscle fibers was surrounded by fibrous tissue, which caused interruption of the "nexus" function and therefore loss of muscle contractions. The inability of normal muscle contractions within the UPJ might be a contributing factor to the pathogenesis of congenital hydronephrosis.

An analysis of forty-two cases of hydronephrosis occurring in a series of 3,400 post mortem examinations (1.2%) shows that bilharzia could not be regarded as a cause of death in any of them. This is evident in thirty of the cases, since bilharzial lesions were not present in these. In the other twelve cases in which bilharzial lesions were present major obstructive diseases (carcinoma of bladder, prostatic obstruction) sufficiently accounted for the hydronephrosis in six cases. This leaves six cases, none of them severe, in which bilharziasis might have played a part, though other causes such as congenital ureteric constrictions cannot be excluded: This type of lesion was present to the same extent in the non-bilharzial as in the bilharzial group of hydronephrosis. It may be concluded that in Zambia at any rate bilharzia does not seriously contribute to advanced hydronephrosis, but may be responsible for some mild, symptomless forms of the disease.

The dependence of pathomorphological changes in the regional lymphatic ganglia of the dog's kidney upon the duration of experimental hydronephrosis is shown. The development of necrosis in some of them points out indirectly to the participation of the renal lymphatic system in carrying off the urine saturated with toxic products persisting in it for a long period. Increased dilatation of intermediate and medullary sinuses is connected with continuous inflow of the lymph that contributes to its congestion and then leads to the retrograde flow. A mechanical obstraction appears on the way of lymph and this fact aggravates mechanical insufficiency of the lymph circulation. At the same time this particular case is lymphogenic sclerosis, which is induced by acumulation of disturbed metabolism products in the intermediate tissue brought by the lymph.

This report describes a human embryo with a length of 12 mm (horizon XVII Streeterm 35 +/- 1 day old), in which the following malformations appear: Dilation on both sides of the Wolffian ducts, and the more caudal mesonephritic glomerules (mesohydronephrosis). Dilatation of both ureters and renal pelvis (uretero-hydronephrosis). These malformations are the result of the accumulation of liquid secreted by the mesonephros in a cloaca which is dilated, unwalled and blocked by an epithelial plug which is continuous with the cloacal membrane.

Focal papillary hyperplasia in the trigone of the urinary bladder caused partial urethral and ureteral obstruction in 4 Holstein-Friesian cows. Secondary chronic hydronephrosis resulted in clinical and laboratory evidence of chronic renal failure.

In a case of an 18-yr-old girl with generalized neurofibromatosis there was an unilateral hydronephrosis due to polypoid neurofibromas in the ureter and urinary bladder. In the kidney were interstitial neurofibromas, a great number of dysontogenetic adenomas and also neurofibromatosis of the vessels.

Four hundred ninety-seven patients representing the 525 total or polar nephrectomies performed at the Children's Memorial Hospital from 1938 to 1973 (excluding 1947), were reviewed retrospectively to determine the incidence and characteristics of renal dysplasia. The 46 specimens with this histologic diagnosis all exhibited typical primitive ducts with 13 being also associated with cartilage formation. In five patients, kidney showed focal chondrous metaplasis of the interstitium in association with chronic inflammation but without primitive ducts. The findings strongly suggest that the renal interstitium occasionally may react to injury by chondrous metaplasia and that, in the absence of primitive, ducts, cartilage in the kidney is not pathognomonic of renal dysplasia.

The clinical features, diagnosis and treatment of 26 adults with primary obstructive megaureter have been reviewed. The histological features and the urodynamics of this disease are discussed. The clinical picture of primary obstructive megaureter in the adult may be deceivingly unimpressive. In this series 2 kidneys were destroyed because of progressive disease in the absence of clinical symptoms. We support Creevy's findings that the pathology involved is an obstructive segment of the ureter on the basis of a thickened muscularis and mild inflammation of the mucosa and submucosa. Urodynamic studies performed by one of us (M.K.H.) suggest that these ureters may remain in a balanced state indefinitely, owing to a low resting pressure. However, there may be relatively little reserve capacity and, with increased urine production rates, the pressure transmitted to the renal collecting system may produce renal atrophy. The radiologic features of the disease may reflect its clinical course, that is those showing a bulb and tail have a more benign course than ureters with a sharp cutoff. High dosage cine-pyelography is valuable in confirming the diagnosis and in studying the contractility of the ureter. Initially, we treated these cases conservatively. The presence of calculi and planned pregnancy are strong indication for surgical interference. Of the 26 patients 15 ultimatley required an operation. We recommend ureteral remodeling and reimplantation whenever possible since 11 of our cases had a most gratifying result from this procedure.

In a review of 156 total or partial nephrectomy specimens from patients over the age of 12 years, renal dysplasia was found 14 times. The cases were divided initially into five groups on the basis of the predominant pathological changes, namely (1) dysplasia (14 cases), (2) chronic pyelonephritis (31 cases), (3) calculous inflammation (58 cases), (4) hydronephrosis (35 cases), and (5) miscellaneous (18 cases). The diagnosis of dysplasia was made on gross and microscopic criteria and included 12 of segmental dysplasia, one of total dysplasia, and one multicystic dysplastic kidney. The principal differential diagnosis is from the irregularly scarred chronic pyelonephritic kidney. The criteria for the separation of the two are emphasized and, in particular, the distinction from those pyelonephritic kidneys with aglomerular scars. A high incidence of anomalies of drainage was found in association with dysplasia, but such were not always present. It was not thought that intrarenal reflux in infancy was an aetiological factor. Six of the cases presented with urinary infection, but only two had hypertension. It was thought that acquired glomerular damage was more important in the aetiology of hypertension than segmental glomerular agenesis.