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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal function was investigated in a group of ten patients aged two months to eleven years, with chronic or recurrent urinary tract infection caused by different malformations of the urinary tract. The following tests were performed: endogenous creatinine clearance, maximal urinary concentrating ability, urinary acidification, maximal urinary diluting ability, free water clearance, index of fractional distal sodium delivery and index of distal tubular reabsorption of sodium. It is concluded that the follow-up of glomerular function by means of creatinine clearance and of tubular function by means of maximal concentrating ability consitute the most sensible way to detect renal functional impairment in children with chronic or recurrent pyelonephritis.
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PMID:[Alterations of renal function in pyelonephritis (author's transl)]. 23 18

Thirty-three patients with acute pyelonephritis were studied with regard to the changes in plasma renin activity (PRA) along the clinical course of the disease. 1) Abnormally high PRA was found in 64% of patients in the active stage of acute pyelonephritis; they showed a decrease in urinary output of sodium, a reduction in creatinine clearance, and high indices of inflammatory activity. 2) The changes of PRA in the course of acute pyelonephritis were negatively correlated to the urinary sodium excretion and creatinine clearance, but positively to the activity of inflammation, serum sodium concentration and the number of E. coli in the urine. PRA returned to normal with the improvement of pyelonephritis. 3) Concerning the mechanism of hyperreninemia in the active stage of the disease, the following three factors may be considered; renal ischemia, negative sodium balance in the body, and inflammation. Of these, the negative sodium balance seems to be the most important. The patients could not take enough foods to maintain their energy and sodium balance because of fever and pain. 4) The significance of resting PRA in acute pyelonephritis might be to reflect the sodium status in the body, but not to be related to hypertension.
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PMID:Elevated plasma renin activity in patients with acute pyelonephritis. 69 21

In patients with chronic renal failure due to glomerulonephritis, pyelonephritis or polycystic kidneys the urinary clearance of free chloramphenicol (C(CHL)) was depressed proportionally to GFR (C(In)). The ordinate intercept of the regression line of C(CHL) on C(In), however, consistently was positive (+3 to +5 ml/min). The fractional excretion of chloramphenicol in renal failure increased from its normal value of 50 percent as an exponential function of the decrease of GFR, and as a linear function of the fractional excretion of water or of sodium. Dietary sodium restriction had no influence on C(CHL) in the patients, while water diuresis, in normal subjects, enhanced the urinary excretion of chloramphenicol. The data suggest that chloramphenicol is reabsorbed by back-diffusion and that increases of the rate of flow of urine and tubular fluid prevent back-diffusion.
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PMID:The effects of functional adaptation of residual nephrons on the urinary excretion of drugs. 73 57

We studied prospectively 18 patients with sodium-losing nephropathy. In 12 patients (66.7 per cent) the sodium-losing nephropathy was owing to obstructions, challenging the hitherto existing concept that the most common cause of the condition is pyelonephritis. The diagnosis of sodium-losing nephropathy is important in urological practice since sodium repletion in these cases shortens significantly the hospitalization and preoperative waiting time.
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PMID:Sodium-losing nephropathy. 75 50

Although a diminished fractional excretion of sodium (FENa) is the hallmark of acute proliferative glomerulonephritis (APGN), an enhanced natriuresis per glomerular filtration rate (GFR) in the chronic phases of this disease has been reported. We studied this adaptive response utilizing two different split-bladder dog models with unilateral, and a third group of dogs with bilateral Masugi's nephritis. Group I. Six dogs with unilateral nonaccelerated APGN studied a mean of 6 days after induction had a mean base-line APGN/intact kidney GFR of 31/50 ml/min (P less than 0.005) and FENa of 0.2/0.75% (P less than 0.005). Acute volume expansion caused a smaller absolute increase in FENa from the APGN kidney, 1.6%, than from the intact kidney, 4.0%, (P less than 0.01). Maximum tubular secretion of rho-aminohippuric acid/GFR (TmPAH/GFR) measured in three dogs was higher in the APGN kidney than intact kidney, 13.1 vs. 9.3 mg/dl. Subsequent studies on three of the six dogs when the disease had become chronic demonstrated a reversal in the pattern of sodium excretion in response to volume expansion. Group II. Six dogs with accelerated unilateral APGN (dogs presensitized to antibody source) studied a mean of 5 days after induction had a mean base-line APGN/intact kidney GFR of 16/57 ml/min and FENa of 0.22/0.12% (P less than 0.1). Contrary to group I, volume expansion caused a greater absolute increase in FENa from the APGN kidney, 5.8%, than from the intact kidney, 2.9% (P less than 0.05). TmPAH/GFR studied in four dogs was similar for both kidneys, 17.9 and 18.5 mg/dl for the APGN kidney and intact kidney, respectively. Group III. Sequential studies were performed on seven dogs with bilateral nonaccelerated APGN. Initially each demonstrated sodium retention and a smaller absolute increase in FENa in response to volume expansion compared to a predisease control study. With disease progression, volume expansion induced a greater absolute increase in FENa than in the control study. We concluded that (a) the fractional excretion of sodium from the APGN kidney will be less or greater than the contralateral intact kidney or control study depending on the severity and/or chronicity of the disease, possibly as the result of morphologic alterations; (b) the degree of extracellular fluid volume expansion is an important variable influencing similarity of glomerulotubular balance between the APGN and contralateral intact kidney; and (c) the "intact nephron hypothesis" applies in a limited fashion to kidneys with APGN in the absence of volume expansion just as it does for kidneys with chronic glomerulonephritis or pyelonephritis.
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PMID:Functional adaptation of nephrons in dogs with acute progressing to chronic experimental glomerulonephritis. 93 95

A metabolic study was performed in 28 patients with bilateral recurrent calcium-containing renal staghorn calculi and chronic pyelonephritis ("obstructive nephropathy"). Fourteen had normal GFR and 14 mild renal insufficiency. Ten normal subjects were used as controls. Under basal conditions, polyuria and negative sodium balance were commonly observed in patients with obstructive nephropathy and normal renal function. After an acute acid load (NH4Cl) an acidifying defect, i.e. high values for urine pH and reduced excretion of titratable acid and ammonium, was observed in 64% of patients with normal GFR and in 71.4% of those with renal insufficiency. During intravenous infusion with neutral sodium phosphate, the urine pH changed little but the rate of excretion of titratable acid increased in direct proportion to that of urinary phosphate in both groups of patients. These results, associated with the finding of normal blood pH in almost all patients, lead to the conclusion that an incomplete Type 1 or "distal" renal tubular acidosis is a frequent complication of obstructive nephropathy secondary to bilateral nephrolithiasis. The anatomical abnormalities of renal tubules and collecting ducts and the superimposed interstitial nephritis might be the pathogenetic factors responsible for the acidifying defect and for the impairment in sodium and water conservation.
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PMID:Renal tubular defects in recurring bilateral nephrolithiasis. 95 42

The present studies have confirmed a severe urinary concentrating defect early in the course of experimental enterococcal pyelonephritis. This defect in maximum concentrating ability was almost completely reversed immediately following indomethacin or sodium meclofenamate intravenously. This effect of indomethacin and sodium meclofenamate was transient and was not associated with a fall in numbers of enterococci per gram of kidney. Injection of indomethacin or sodium meclofenamate in noninfected rats had no effect on maximum renal concentrating ability. The potential mechanisms by which indomethacin and sodium meclofenamate, inhibitors of renal prostaglandin synthesis, could reverse a defect in maximum urinary concentration are discussed.
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PMID:Effect of indomethacin and sodium meclofenamate on the renal concentrating defect in experimental enterococcal pyelonephritis in rats. 99 47

After serum creatinine levels exceeded 10mg/100ml, median survival was 55 days (to death or dialysis) in a group of 112 patients with chronic renal disease. Renal failure was partially reversible in 29 patients, partially accounting for prolonged survival. Those with polycystic kidneys, pyelonephritis, or obstructive nephropathy survived longer,partially because of more frequent reversibility and a slower increase in serum creatinine concentration. Kiabetic nephropathy, myelomatous kidneys, and amyloidosis were associated with shorter survival, less frequent reversibility, and more rapid progression. Urinary infection and extracellular volume depletion often accounted for partially reversible renal failure and prolonged survival. Blood pressure and age were not prognostic variables, while coexistent heart failure shortened survival. Survival correlated significantly with sodium excretion.
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PMID:Prognosis of chronic renal failure. II. Factors affecting survival. 114 31

Plasma aldosterone, plasma renin activity, sodium and potassium in the plasma and the urine were determinated under acute stimulation with saline-depletion (furosemide) and under acute suppression with saline infusion in 40 patients with primary hypertension stage I, 19 patients with primary hypertension stages II and III, and 11 patients with renal hypertension (chronic glomerulonephritis and chronic pyelonephritis). The majority of the patients with primary hypertension stage I showed a good stimulation of the plasma aldosterone and the plasma renin activity under acute salt depletion. Three out of the 40 patients with primary hypertension stage I, and 13 of the 19 patients with primary hypertension stages II and III did not show any stimulation of the renin secretion ("low renin hypertension"). In all these patients the plasma aldosterone stimulation remained intact. With infusion of saline all the groups showed suppression of the plasma aldosterone and the plasma renin activity. A good stimulation of the plasma renin activity, demonstrates that in our experiments the renin-angiotensin system cannot be responsible for the increase in aldosterone secretion under salt depletion. Most likely the increase of the plasma aldosterone, in spite of the fixed renin activity, is stimulated by the sodium depletion due to diuretics. In all patients with primary hypertension we did not find an inadequate reaction of the aldosterone secretion under saline infusion. The patients with renal hypertension showed a minimal stimulation and suppression of the plasma renin activity. The plasma aldosterone secretion increased only slightly under sodium depletion and the decrease under saline infusion was statistically not significant. Thus we conclude that these patients show an inadequate reaction of the plasma aldosterone and renin secretion under salt infusion and depletion.
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PMID:[Plasma aldosterone and plasma renin activity in patients with essential and renal hypertension under acute stimulation with saline depletion and acute suppression with saline infusion]. 115 49

It is apparent that the split function study and renal vein renin determination are complementary and afford valuable information for selecting patients with potentially curable renovascular hypertension. The split function study, when interpreted with the recently defined split function ratio, offers the clinician a highly accurate means of diagnosing significant renal ischemia. Because the split function ratio shows the disparity between the ischemic and contralateral kidney to a greater degree, the chance of misdiagnosis due to laboratory or physician error is minimized. The split function study, however, is of limited value in patients with pyelonephritis since the water- and salt-losing characteristics of the pyelonephritic kidney may mask significant renal ischemia. In these patients, as well as those with a nonfunctioning kidney or hydronephrosis, the renal vein renin determination is the test of choice. In addition, the added morbidity of the split function study is not warranted in a patient with an elevated peripheral renin which, for interpretation, requires an accurate 24 hour urine for sodium, a renal vein renin ratio outside the range of patients with essential hypertension (renal vein renin ratio greater than 1.7) and evidence of suppression of renin secretion from the contralateral kidney. If, however, the renin determination does not afford convincing evidence of significant renal ischemia in a patient with radiographic evidence of renal arterial stenosis, a split function ratio definitely should be determined to more completely define the pathology. The attendant morbidity of a carefully performed split renal function study does not approach the morbidity and mortality associated with unnecessary surgery or inadequately treated hypertension.
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PMID:Ureteral catheterization studies. 115 55


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