Relation of Pyelonephritis and Other Urinary-Tract Infections to Arterial Hypertension

Weiss, Soma; Parker, Frederick B.

doi:10.1056/nejm194012122232401

Cited by 26 publications

(4 citation statements)

References 3 publications

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“…As such, it could be the bacterial provocation that has been sought to initiate the immune cascade. The same subtle streptococcal bacteriuria could fulfill the pre diction of Bumpus and Meisser [38], Longcope [39] and Weiss and Parker [40] that underlying the recurrent florid gram-negative bacillary pyelonephritis would be a subtle (nonremitting) hematogenous streptococcal bacteriuria. The same bacteremia-bacteriuria could also account for the progressive loss of renal function in patients with known pyelonephritis who do not have a recurrence of 105 cfu/ml bacteriuria [41], and it would reopen the question of a role for bacteriuria (not necessarily 'pyelonephritis') in hyper tension [39,42,43], a role set aside by the IO5 criterion.…”

Section: Discussionmentioning

confidence: 98%

Computer Algorithm Offers a Comprehensive View of Quantitative Bacteriuria

Hyman¹

1993

Nephron

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Using improved microscopy of urine sediment, the consistent finding of bacteria, usually gram-positive cocci at low counts, free or even in casts, in the sediment of carefully collected urines from patients with systemic illnesses has led to the need to reconsider their exclusion by the customary criteria for ‘significance’ of bacteria in urine. Since ‘significance’ is currently based upon mathematical assumptions limited to high counts ( > 10⁵ colony-forming units/ ml) for the prediction of clinical pyelonephritis alone, a digital computer program was created to predict the full spectrum of the expected concentration of bacteria in bladder urine versus time for a very wide range of possible bacterial division times, bladder kinetics and urine flow rates. Curves generated resulted in the discovery of very simple rules based on an easily calculated discriminant, the host’s critical division time (CDT) for any bacterial species in his urine. (1) If the division time in the urine of a species entering the urinary tract is shorter than the CDT, the bacteria will proliferate to > 10⁵ cfu/ml. Published data on growth in human urine show that very few bacterial species can divide so fast in urine, and those are the ones currently considered ‘significant’. Except for some enterococci, streptococci cannot. (2) With a division time only marginally longer than the CDT, any bacterium would wash out unless continuously supplemented via the kidney or from the bladder wall. (3) With a continued supplement and the longer division time, the concentration would fall to a low plateau, and that plateau is diagnostic of a continued supplement. The cocci observed by microscopy are fastidious or dead. They grow poorly if at all in urine, and thus are not likely to ascend the urinary tract. Their appearance corresponds to the earlier studies of bacteriuria and to the known excretion of blood-borne bacteria in natural disease, whether or not there are anatomical changes in the kidney. It is suggested that the low-level coccal bacteriuria found is a marker for scant bacteremia in many systemic diseases for which a bacterial provocation has been sought.

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Section: Discussionmentioning

confidence: 98%

Computer Algorithm Offers a Comprehensive View of Quantitative Bacteriuria

Hyman¹

1993

Nephron

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“…In linking chronic pyelonephritis to arterial hypertension, the role of renal ischemia originating from obstructive endarteritis as proposed by Weiss and Parker [14] has long been considered important. Kincaid-Smith [5] showed an ischemic parenchymal lesion called ischemic tubular atrophy, which was correlated with high blood pressure and most commonly associated with a marked decrease in renal mass.…”

Section: Discussionmentioning

confidence: 99%

“…From these results it was concluded that experimentally induced chronic pyelonephritis in dogs caused a rise in blood pressure. No connection be tween the pyelonephritis and the renin angiotensin system was found.The clinical relationship between chronic pyelonephritis and hypertension was noted early by Longcope [7] and Weiss and Parker [14]. Spitznagel and Schroeder [9] produced unilateral Escherichia coli pyelonephritis in rats with one ligated ureter and found hypertension in a significant number of animals.…”

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confidence: 99%

Hypertension and Plasma Renin Activity in Experimentally Induced Chronic Pyelonephritis

Tsuchida¹,

Yamaguchi²,

Arai³

et al. 1976

Nephron

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The present authors conducted a series of experiments with mongrel dogs, in which unilateral chronic pyelonephritis was induced and postoperative changes in blood pressure and plasma renin activity were observed over a period of 3 months. The pyelonephritis infection was brought about by a method involving vesicoureteral reflux and ureteral dysfunction, as described in a previous paper. Pre- and postoperative levels of systolic pressure were compared, but no definite trends were found for the first 3 weeks after operation. At 30, 60 and 90 days the pressures were found to have risen by 21.2 ± 14.6 and 17.1 ± 16.7 mm Hg, respectively. No appreciable change in the plasma renin activity was found, however, at any stage. From these results it was concluded that experimentally induced chronic pyelonephritis in dogs caused a rise in blood pressure. No connection between the pyelonephritis and the renin angiotensin system was found.

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“…The clinical relationship between chronic pyelonephritis and hypertension was early noted by Longcope (1937) and Weiss and Parker (1940). Experimentally, Spitznagel and Schroeder (1951) induced pyelonephritis unilaterally in 16 rats by partial ureteral con striction and intravenous injection of E. coli, and confirmed resultant hypertension in 9 cases.…”

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confidence: 86%