Patterns of nephron perfusion in acute and chronic hydronephrosis.

Suki, Wadi N.; Eknoyan, Garabed; Rector, Floyd C.; Seldin, Donald W.

doi:10.1172/jci105316

Cited by 88 publications

(30 citation statements)

References 20 publications

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“…These workers produced a variety of unilateral renal lesions including pyelonephritis and aminonucleoside nephritis. Suki et al also observed an increase in fractional salt and free water excretion in chronically hydronephrotic dogs (8). The functional similarity in this disparate group of pathological conditions suggests some common unifying feature.…”

Section: Resultsmentioning

confidence: 90%

“…The predominant locus of damage has been variously assigned to both the proximal (1,2) and distal (3-7) nephron. Suki, Eknoyan, Rector, and Seldin (8) in a study of unilateral chronic hydronephrosis in hydrated dogs have concluded that the major disturbance in the obstructive nephropathy is increased GFR (glomerular filtration rate)1 per nephron leading to decreased proximal tubular reabsorption of sodium and hyperperfusion of the distal nephron. They further suggested that back-diffusion of solute free water was impaired in the collecting duct and possibly in the descending limb of Henle's loop by anatomic disruption of medullary tissue thereby permitting excessive urinary dilution.…”

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confidence: 99%

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The postobstructive kidney. Observations on nephron function after the relief of 24 hr of ureteral ligation in the dog

Bercovitch¹,

Kasen²,

Blann³

et al. 1971

J. Clin. Invest.

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A B S T R A C T After the relief of 24 hr of complete unilateral ureteral obstruction in the dog, the experimental kidney is characterized by a decrease in filtration rate and an increase in fractional and often absolute excretion of sodium before and after the administration of mannitol. In the hydrated state, the failure to conserve sodium is associated with increases in fractional free water clearance and fractional sodium supply to waterfreeing sites signifying that the augmented sodium excretion is derived from a proximal source. In the hydropenic state there is decreased fractional free water reabsorption, and sometimes free water excretion, in the postobstructive kidney. An early plateau in free water reabsorption is associated with an increased fractional excretion of sodium. These findings are attributed to the early development of distal nephron impermeability to water as a result of enhanced distal tubular supply and transport of sodium. There is a decrease in maximal tubular reabsorptive capacity (Tm) of glucose in the postobstructive kidney which is, however, less marked than the decrease in filtration rate. The fall in filtration rate is to some extent likely due to a dropping out of nephrons from the circulation while the remaining nephrons are hypoperfused. The magnitude of the sodium reabsorptive defect is markedly exaggerated as the concentration of nonreabsorbable solute (mannitol) in the glomerular perfusate is increased. It is concluded that the postobstructive increase in sodium excretion during mannitol adThis work was presented at

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Section: Resultsmentioning

confidence: 90%

mentioning

confidence: 99%

The postobstructive kidney. Observations on nephron function after the relief of 24 hr of ureteral ligation in the dog

Bercovitch¹,

Kasen²,

Blann³

et al. 1971

J. Clin. Invest.

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“…The reason for the lower GFR is not certain but may be-related to the fact that water was withheld from our experimental animals for 24 hr whereas patients with the * postobstructive syndrome are usually not dehydrated and are often overhydrated. The site of impaired sodium reabsorption is unknown in either man or experimental animals but on the basis of clearance data various investigators have assigned it to either the proximal (3,6,(27)(28)(29) or the distal tubules (1,4,5).…”

Section: Methodsmentioning

confidence: 99%

A Micropuncture Study of Postobstructive Diuresis in the Rat

Yarger¹,

Aynedjian²,

Bank³

1972

J. Clin. Invest.

100

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A B S T R A C T In order to investigate the syndrome of postobstructive diuresis, clearance and micropuncture studies were carried out in rats after relief of 24 hr of bilateral (BUL) or unilateral (UUL) ureteral ligation. In rats with BUL, a striking diuresis and natriuresis occurred when the obstruction to one kidney (the experimental kidney) was relieved. The results were not influenced by administration of vasopressin or d-aldosterone. Whole kidney clearances of inulin and p-aminohippuric acid (PAH) in the experimental kidney were reduced to 10% and 20% of normal, respectively. Superficial nephron inulin and PAH clearances were also reduced, but only to 40% and 45%, respectively. These findings suggest a heterogeneity of nephron function in which deep nephrons were functioning poorly or not at all. To investigate the site of impaired tubular reabsorption in the surface nephrons, absolute and fractional water reabsorption was measured. Absolute reabsorption was found to be decreased all along the nephron. Fractional reabsorption in proximal tubules was normal, as indicated *by an average endproximal tubular fluid per plasma inulin (TF/Pi.) of 2.16 vs. 2.30 in controls. TF/Pri was markedly decreased in distal tubules (2.91 vs. 8.02) and final urine (5.56 vs. 263). These observations indicate that the major sites of impaired sodium reabsorption leading to the diuresis were beyond the proximal tubule.

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“…An immuneniediated etiology has been postulated on the basis of the demonstration of complement and immunoglobulin in the affected glomeruli [51,52], The antigenic stimulus for this presumed process is as yet unknown. However, it has been postulated that VUR may release immunogenic proteins (such as Tamm-Horsfall protein) into the circu lation, initiating the formation of autoantibodies and immune complexes [51,56,57], Others have challenged this proposed immune mechanism for the development of focal glomerulosclerosis [10,57,58], Rather, it was speculated that the lesions may be secondary to adaptive hemodynamic changes which have been shown to occur in hypertrophied nephrons [57,59,60]. These adaptive hemodynamic changes have been demonstrated in a model of chronic hydronephrosis in which reduced renal mass is associated with overperfusion of residual neph rons and a presumed increase in glomerular filtration rate per nephron [59].…”

Section: Significance Of Refluxmentioning

confidence: 99%

“…However, it has been postulated that VUR may release immunogenic proteins (such as Tamm-Horsfall protein) into the circu lation, initiating the formation of autoantibodies and immune complexes [51,56,57], Others have challenged this proposed immune mechanism for the development of focal glomerulosclerosis [10,57,58], Rather, it was speculated that the lesions may be secondary to adaptive hemodynamic changes which have been shown to occur in hypertrophied nephrons [57,59,60]. These adaptive hemodynamic changes have been demonstrated in a model of chronic hydronephrosis in which reduced renal mass is associated with overperfusion of residual neph rons and a presumed increase in glomerular filtration rate per nephron [59]. More recently, in a model of ablation of eleven-twelfths of the renal mass, residual nephrons dem onstrated a marked increase in single nephron glomerular filtration rates with greatly augmented glomerular pres sures and flows [60], Structural abnormalities of all glo merular cell types were associated with these hemody namic changes.…”

Section: Significance Of Refluxmentioning

confidence: 99%

Vesicoureteral Reflux and Reflux Nephropathy

Senekjian

Suki

1982

Am J Nephrol

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Vesicoureteral reflux is an anatomic abnormality, mostly affecting a pediatric population, which may be the second leading cause of end-stage renal failure. Most cases of reflux are due to abnormalities in the insertion of the ureters into the bladder, either congenital or acquired. Most commonly, VUR is discovered during routine evaluation of urinary tract infections, but may also be present in patients with severe hypertension or chronic renal failure. The diagnosis is confirmed radiologically, utilizing either voiding cinecystography or radioisotopic methods. VUR can result in renal failure through scarring secondary to ‘chronic pyelonephritis’ or through a glomerulopathy, possibly immune in origin. In most series, the glomerulopathy is felt to be the cause of the end-stage renal failure. Treatment of VUR includes conservative (medical) management with the hope that maturation of the ureterovesical junction will cure reflux. Surgical therapy is reserved for those patients in whom this maturation is not expected to occur or in those whose urinary infections cannot be controlled. In those patients who have developed the glomerulopathy secondary to VUR, surgery may not halt the progression of the renal disease. VUR in a transplanted kidney may result in a higher risk of loss of the graft due to glomerulopathy or chronic rejection.

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Patterns of nephron perfusion in acute and chronic hydronephrosis.

Cited by 88 publications

References 20 publications

The postobstructive kidney. Observations on nephron function after the relief of 24 hr of ureteral ligation in the dog

The postobstructive kidney. Observations on nephron function after the relief of 24 hr of ureteral ligation in the dog

A Micropuncture Study of Postobstructive Diuresis in the Rat

Vesicoureteral Reflux and Reflux Nephropathy

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