Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Trigonal-colonic anastomosis for diversion of urine into the colon was performed in 12 clinically normal dogs and in 10 incontinent dogs with diseases of the urinary bladder or urethra. Dogs were studied from 1 to 30 months after surgery. The surgical procedure was technically satisfactory. Fifteen of 22 dogs were studied with intravenous urography, and only 1 case of hydronephrosis was found. Pyelitis was a common histopathologic finding in both groups of dogs. Pyelonephritis developed in 30% of dogs, regardless of duration of anastomosis. Glomerular filtration rate was reduced in all dogs studied, but renal failure was infrequent. Values for blood urea nitrogen and serum inorganic phosphorus were elevated due to intestinal recycling of nitrogenous products and phosphate. Electrolyte imbalances were not a problem, but gastrointestinal disturbances developed in 3 of the 10 diseased dogs. Six of 10 diseased dogs survived from 9 months to more than 3 years. Trigonal-colonic anastomosis appears to be a satisfactory salvage procedure for incontinent dogs with diseases of the urinary bladder or urethra that do not respond to other forms of therapy.
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PMID:Trigonal-colonic anastomosis: a urinary diversion procedure in dogs. 44 50

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 term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

The authors report about 12 cases of long ureteral calculi, 16 to 39 mm in size, observed over 10 years. They were all made of a mixture of ammonium-magnesium phosphate and calcium phosphocarbonate. Infection was the revealing symptom, either in the form of simple bacteriuria or as acute pyelonephritis or sepsis. These calculi, found in a lumbar or pelvic location, were very long, radiopaque but with a moderate radiological density, homogeneous and have regular contours. They were straight, sometimes slightly bent, rarely (one case out of 12) arciform. In 11 of 12 cases, the affected patient was female. In most cases, the urine was infected by Proteus mirabilis. In spite of their size, the calculi caused total obstruction in 3 of 12 cases only. They were or were not associated to ipsilateral coral calculi of the same chemical type. Destruction was easily achieved with physical agents. The etiological, radiological and therapeutic characteristics of these calculi give them a specific place among ammonium-magnesium phosphate calculi.
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PMID:[Long ureteral ammonium-magnesium phosphate (struvite) and calcium phospho-carbonate calculi]. 180 76

Patients with pyelonephritic renal scarring are at risk of developing renal failure and hypertension. We studied glomerular filtration rate (GFR), renal plasma flow (RPF), filtration fraction (FF), systolic (SBP) and diastolic (DBP) blood pressure, fractional sodium, potassium and phosphate excretion, peripheral renin activity (PRA), plasma aldosterone (p-Aldo), urinary albumin excretion (U-Alb) and urinary beta 2-microglobulin excretion (beta 2-M) in hydropenia and during transition to 3% volume expansion with isotonic saline infusion in 22 female patients with renal scarring due to pyelonephritis and 9 healthy controls. The patients had significantly lower GFR, higher SBP and higher PRA in hydropenia, but there was no significant difference in RPF, FF, DBP or p-Aldo. After volume expansion, SBP, DBP, PRA and p-Aldo were significantly higher in patients than in controls. Transition to 3% volume expansion was associated with a similar increase in SBP in both patients and controls, whereas DBP increased significantly more in the patients (p less than 0.01). Volume expansion resulted in a significant suppression of PRA and p-Aldo in both patients and controls. The patients with renal scarring had the same capacity to excrete sodium and water during transition to volume expansion as the healthy controls. The renin-aldosterone system seems abnormally activated and is probably more important than hypervolemia in the development of hypertension in this group of patients.
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PMID:Role of hypervolemia and renin in the blood pressure control of patients with pyelonephritis renal scarring. 304 33

Renal tubular function tests were performed in 45 children suffering from upper and lower urinary tract infections. Determinations were made of the urinary carbon dioxide tension in maximally alkaline urine as an index of distal tubular H+-ion secretion, of urinary protein excretion, and of urinary sodium and phosphate handling. Urinary PCO2 was low (2.7 +/- 13.9 mmHg) in acute pyelonephritis compared to values in healthy children (52 +/- 32 mmHg) or those with cystitis (48 +/- 34 mmHg). At the onset of pyelonephritis an elevated fractional excretion of sodium (1.38 +/- 0.38 vs. 0.50 +/- 0.20%) and decreased phosphate reabsorption (69.2 +/- 7.1 vs. 90.4 +/- 4.9%) were also observed. Significantly elevated urinary low molecular weight protein excretion was also found in pyelonephritis. These data indicate the existence of proximal and distal tubular dysfunction at the onset of acute bacterial pyelonephritis.
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PMID:Alterations of urinary carbon dioxide tension, electrolyte handling and low molecular weight protein excretion in acute pyelonephritis. 308 6

The progression of renal failure was analyzed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosuppressive treatment. The reciprocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephropathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p less than 0.01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration. For those with linear progression of renal failure there was a significant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure. Calcium phosphate product correlated poorly with the rate of deterioration. We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure. Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephritis.
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PMID:Renal pathology and proteinuria determine progression in untreated mild/moderate chronic renal failure. 320 6

To clarify the relationship between urinary tract infections and stone formation, infected renal calculi removed surgically from 19 patients were investigated. First, the stones were studied using a scanning electron microscope and bacteriological method. Most of the stone cores consisted of calcium phosphate and organic materials containing bacteria, fibrin, erythrocytes, leukocytes and so on. Second, in experimental ascending pyelonephritis in rats which received the intravesical instillation of Proteus mirabilis, the incidence of renal stone formation was increased with the grade of the pyelonephritis and necrotic papillae played an important role as stone nuclei. Third, urinary materials, which may initiate and accelerate stone formation, were investigated using the urine of stone formers associated with renal infections, nucleopore filters and stitches, from the standpoint of crystal aggregation and adhesion effects. The bacteria tended to aggregate crystalline and organic matters in the urine and to adhere them to the stitches before the crystals. The results obtained suggest that the bacteria and organic matters in the urine of stone formers participate actively in stone genesis and growth as an adhesive agent.
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PMID:[Renal infections and implicated urinary stone formation]. 390 92

Bone morphological parameters of renal osteodystrophy such as abundance of osteoid surface, osteoid seam width index, calcification fronts, osteoclast activity and trabecular bone volume were studied in 71 patients on maintenance hemodialysis and compared with bone densitometry, laboratory and clinical data. Increased osteoclast activity (hyperparathyroidism) was by far the most common bone morphological finding. Patients with chronic pyelonephritis or polycystic kidney disease had more than double the amount of osteoid than patients with chronic glomerulonephritis. The trabecular bone volume seemed to be increased in most patients in contrast to the cortical bone volume which was decreased, judged from bone densitometry and previously from X-ray. Despite that patients with polycystic kidney disease were older, their trabecular volume was larger than in patients with glomerulonephritis. The bone mineral content evaluated by bone densitometry was low in most patients, and more associated with bone morphological signs of osteomalacia than with secondary hyperparathyroidism. Serum phosphate (S-PO4) and serum parathyroid hormone (S-PTH) seemed to discriminate better between osteomalacia and secondary hyperparathyroidism than serum alkaline phosphatase (S-Alk. phosph.), which was elevated in both groups. Patients who had been bilaterally nephrectomized were no more abnormal than other patients, and they had lower S-Alk. phosph. The abundance of osteoclasts was found to be a predictor of future development of clinical secondary hyperparathyroidism.
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PMID:Studies of bone morphology, bone densitometry and laboratory data in patients on maintenance hemodialysis treatment. 397 74

Of nine patients with uraemic osteomalacia, the underlying renal lesion was pyelonephritis in seven. All of the patients were characterized by impairment of acidifying power and severe metabolic acidosis. It is suggested that metabolic acidosis may be a definite factor in the pathogenesis of uraemic osteomalacia, possibly by reducing the proportion of trivalent phosphate in the plasma and/or by reducing plasma calcium.
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PMID:Role of acidosis in renal osteomalacia. 578 Apr 54


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