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

Depletion of potassium is common in old people and is due to abnormal urinary excretion (misuse of diuretics, chronic pyelonephritis), to increased faecal elimination (misuse of laxatives, chronic diarrhoea) or to inadequate dietary intake. In a series of 90 elderly patients whose potassium status was investigated, the main manifestations of potassium deplition were weakness, increased sensitivity to digitials, impaired glucose tolerance and mental confusion. Potassium depletion can be most easily demonstrated by measurement of red-cell potassium levels; this method provides a valuable indication of the intracellular potassium content.
 ...
PMID:Potassium depletion in aged patients: an evaluation through red-blood-cell potassium determination. 55 56

Case report on a 35-year-old female patient with life-threatening respiratory insufficiency in extreme hypopotassemia with unclear genesis. A simultaneously existing systemic acidosis and alkaline urine render a secondary tubular acidosis as a sequel of a symptom-poor chronic pyelonephritis probable. Ascertainment by ammonium chloride load. Discussion of the most essential causes of a hypotassemia and emphasizing of a consequent antibiotic sanation also of asymptomatic bacteriurias. It is referred to the necessity of a highly dosed long-term potassium substitution.
 ...
PMID:[Renal potassium-loss syndrome as origin of extreme hypokalemia]. 66 10

A case of Turner's syndrome is presented; many congenital defects were detected. Predominant clinical findings were cheilognatoschisis, respiratory distress, caused by congenital bronchiektasis and chronic hypokalemia with paroxysmal attacks of paralysis and tetania. Hypokalemia was mainly due to gastrointestinal losses as a consequence of permanent vomiting in the presence of stomach atonia and hiatus insufficiency or because of "third space losses", while a subileus persisted chronically. Furthermore also a renal loss of serum potassium was evident in the patient's predialytic time. Basic renal diseases were pyelonephritis, renal damage from phenacetine abuse, or probably even a nephropathy due to potassium depletion. Uraemia was controlled by dialysis treatment and by a dialysate consisting of 7 and 6 mmol/l potassium respectively. The result of this intense therapy was physical rehabilitation and the patient finally could resume her professional work again.
 ...
PMID:[Intractable renal and enteral loss of potassium in a case of Turner's syndrome (author's transl)]. 72 52

The clinical presentations and renal biopsy specimens of 18 patients with primary aldosteronism were reviewed to determine the characteristic pathologic features of the kidney in this syndrome. All patients were hypertensive with a mean blood pressure of 192 nm. Hg systolic and 122 mm. Hg diastolic. The average duration of hypertension was 6.88 years. The mean serum potassium was 2.88 mEq. per l. and the mean plasma carbon dioxide was 31.4 mEq. per l. A significant history of urinary tract disease was noted in 8 patients. Laboratory and diagnostic studies evaluating renal structure and function were abnormal in 11 patients. Renal biopsies from all 18 individuals showed evidence of parenchymal damage. Hypertensive and hypokalemic changes were the most significant abnormalities and were considered moderate to severe in 78 and 89 per cent of the patients, respectively. Histologic evidence of pyelonephritis was noted in 2 patients only and no renal specimens contained characteristic changes of metabolic alkalosis. The preoperatively hypertensive and renal evaluations did not reflect the severity of the renal changes noted histologically. The extent of renal injury caused by hypertension and hypokalemia in these patients emphasizes the consequences of primary aldosteronism. Early diagnosis and treatment of this disorder are essential if these consequences are to be avoided.
 ...
PMID:Renal changes in primary aldosteronism. 83 53

The symptoms and clinical course of chronic hypokalemic nephropathy are described in 21 patients with longstanding potassium deficiency. In 14 patients (group A) the potassium depletion was caused by malnutrition and/or abuse of laxatives and/or diuretics. 7 patients (group B) suffered from primary (6 cases) or secondary (1 case) aldosteronism. The average duration of potassium depletion was 8.8 years in group A and 3.4 years in group B. Depending on the duration of potassium depletion, chronic renal disease develops which may end in terminal renal failure. Urinalysis is non-specific or negative. The clearance of creatinine slowly decreases. Metabolic alkalosis is a constant finding and in group A occurs with a tendency to hyponatremia and hypochloremia, with the development of metabolic acidosis only in advanced renal insufficiency. In contrast to patients of group B, patients of group A have normal or low blood pressures converting to hypertension, if at all only in the late phase. The cases of group A had secondary aldosteronism (and, correspondingly, a hyperplastic juxtaglomerular apparatus). Although urinary tract infection is a regular finding in advanced stages, the clinical, radiological and histological evidence suggests that bacterial pyelonephritis, if occurring at all, is rather a complication than the cause of the disease. In 5 patients 7 instances of acute renal failure of unknown origin were observed which was lethal in one case. Another patient died from terminal renal failure, a third from an intercurrent pneumonia. Renal histology obtained from 13 patients showed the picture of diffuse chronic abacterial interstitial nephritis.
 ...
PMID:Symptoms and course of chronic hypokalemic nephropathy in man. 87 Feb 67

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.
 ...
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

The present study demonstrates that renal tubular unresponsiveness to aldosterone, without associated hyperkalaemia, is present in children with acute pyelonephritis. We studied 32 children with a diagnosis of acute pyelonephritis established by high fever, flank pain/tenderness, increased blood levels of C-reactive protein and significant Escherichia coli growth in the urine culture. Renal tubular function tests and determinations of plasma renin activity and aldosterone concentration were performed at diagnosis (study 1), after three days of iv gentamycin (study 2) and after 21 days of antibiotic therapy (study 3). Findings were compared to those present in 32 normal children of similar age. Despite normal plasma potassium concentration, fractional potassium excretion and transtubular potassium concentration gradient were significantly decreased in studies 1 and 2, becoming normal in study 3. Decreased renal potassium excretion coexisted with increased values for plasma renin activity and aldosterone concentration. In study 3 these hormones remained elevated only in patients with scarred kidneys. The functional alteration present in acute pyelonephritis may be directly caused by the interstitial inflammation or be mediated by some E. coli endotoxin.
 ...
PMID:Normokalaemic pseudohypoaldosteronism is present in children with acute pyelonephritis. 149 6

Renal transportation of sodium and potassium was studied in 85 patients who sustained hemorrhagic fever complicated with renal syndrome (HFRS). The examinees were given routine diet No. 7 recommended by Pevzner. The conclusions were made on the analysis of circadian excretion and clearance of electrolytes studied and the levels of their water-load-induced tubular transportation: distal and proximal reabsorption and distal excretion of sodium, the correlation between potassium secretion and reabsorption in the distal part of the nephron. It was revealed that within the first year after the disease onset, 37.5 per cent of patients had increased levels of sodium excretion as part of the salt-loss syndrome developed due to decreased sodium reabsorption in the distal part of the nephron. Later the status was featured by moderately pronounced disorders of distal sodium reabsorption in 6.25 per cent of the patients only, mostly in those with HFRS-induced pyelonephritis. Increased excretion of potassium noted in the first months after HFRS only was the result of an increase in sodium excretion. The aforementioned disorders could be easily compensated by a routine diet and therefore a decrease in the levels of sodium or potassium avoided.
 ...
PMID:[Electrolyte excretion in patients with a history of hemorrhagic fever with renal syndrome]. 197 Sep 13

Structural aspects of copper chloride crystallization of the urine of patients with pyelonephritis and glomerulonephritis were studied by electron microscopy. It was found that admixtures of urea, creatinine, potassium and, possibly, sodium contained in the urine of patients initiate the formation of copper chloride crystals of different sizes, their shape changes, dendritic and spherolithic crystallization occurs. Results may be used as supplementary differential diagnostic signs of glomerulonephritis and pyelonephritis.
 ...
PMID:[A crystallographic method in the diagnosis of kidney diseases]. 209 91

Diagnostic potentialities of the crystallo-optic++ analysis of cupric chloride crystallographs++ were studied in 76 children with pyelonephritis and in 50 children with glomerulonephritis. The structural and morphological characteristics of cupric chloride crystallization under the influence of the urine from children with pyelo- and glomerulonephritis may serve as the additional differential-diagnostic signs of the diseases. The use of raster electron microscopy widens the diagnostic potentialities of the crystallographic method. Different dimensions of the little crystals formed as a result of isomorphic replacement of copper atoms by potassium ions (and, possibly, by sodium ions) and in the presence of urea and creatinine underlie the differences in cupric chloride crystallographs.
 ...
PMID:[Diagnostic possibilities of a crystallographic method in pyelonephritis in children]. 239 67


1 2 3 4 5 Next >>