Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with excessive industrial exposure to silicon and an elevated silicon content in his renal tissue was found to have a distinctive nephropathy, characterized pathologically by changes in the glomeruli and proximal tubules, and manifested clinically by albuminuria and hypertension. Proximal tubular function was intact. From a biochemical standpoint, this finding correlates with the demonstration in vitro that, in contrast to cadmium, a known cause of Fanconi syndrome, silicon does not inhibit renal cortical sodium-potassium-adenosine triphosphatase (Na-K-ATPase).
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PMID:Silicon nephropathy. 113 57

One hundred and ninety-three nephrotic children with a total of 271 admissions during the past decade, from 1980 to 1989, were retrospectively reviewed for acute complications and unusual features of nephrotic syndrome. One hundred and forty-nine patients were male, 44 female. Hypertension was found in 41 children (21.2%). Nine patients (4.7%) had a total of 11 episodes of hypovolemic shock. These shock patients had a more severe hemoconcentration (mean hemoglobin concentration 19.6 +/- 1.5 g/dl) and hyponatremia (mean serum sodium 127.5 +/- 8.5 mmole/L). Bacterial infections occurred in 28 children (14.5%) with primary peritonitis in 13, sepsis in 6, cellulitis in 4, urinary tract infection in 4 and osteomyelitis in 1. Almost all infections were caused by gram-negative bacilli. Other complications or features included tetany in 4 (2.1%), thromboembolism in 2 (1.0%), pancreatitis in one (0.5%) and Fanconi syndrome in one (0.5%).
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PMID:Complications of nephrotic syndrome in children. 168 Oct 1

The potential role of trace metals in the pathogenesis of various disease states, especially of renal and cardiovascular disease, has been recognized increasingly. Moreover, altered membrane transport was recently incriminated to play a role in renal tubular syndromes, such as the Fanconi syndrome, as well as in the pathogenesis of volume dependent hypertension. We therefore investigated the possible in vitro effects of various trace metals on Na-K-ATPase, the biochemical correlate of active cellular transmembrane sodium and sodium-dependent transport. To more closely mimic the in vivo situation, we deliberately chose as enzyme source renal tissue homogenate, which may contain protective agents. Under these experimental conditions, the metals studied inhibited the enzyme quantitatively in the following order: Hg greater than Pb greater than Cd greater than Ur greater than Cu greater than Zn greater than Mn greater than Ba greater than Ni greater than Sr. Enzyme kinetic studies showed that Hg, Pb, and Cd competitively, and Cu noncompetitively, inhibited the enzyme. In general, Mg-ATPase was significantly less sensitive to the trace metals. Accumulation of these metals may present serious health hazards by producing a general defect in cell membrane transport. From the other metals studied, i.e., Mn, Ba, Ni and Sr, some may have toxic effects via other mechanisms, whereas some may exert a protective role against toxicity of other agents including metal ions.
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PMID:In vitro inhibition of Na-K-ATPase by trace metals: relation to renal and cardiovascular damage. 302 55

IN TWO PATIENTS WITH CLASSIC RENAL TUBULAR ACIDOSIS (RTA) AND IN TWO PATIENTS WITH RTA ASSOCIATED WITH THE FANCONI SYNDROME, RENAL POTASSIUM WASTING PERSISTED DESPITE SUSTAINED CORRECTION OF ACIDOSIS: (a) during moderate degrees of hypokalemia, daily urinary excretion of potassium exceeded 80 mEq in each patient; (b) during more severe degrees of hypokalemia, daily urinary excretion of potassium exceeded 40 mEq in two patients and 100 mEq in another. These urinary excretion rates of potassium are more than twice those observed in potassium-depleted normal subjects with even minimal degrees of hypokalemia. The persistence of renal potassium wasting may have resulted in part from hyperaldosteronism, since urinary aldosterone was frankly increased in two patients and was probably abnormally high in the others relative to the degree of their potassium depletion. The hyperaldosteronism persisted despite sustained correction of acidosis, a normal sodium intake, and no reduction in measured plasma volume, and was not associated with hypertension; its cause was not defined. In the two patients with classic RTA, neither renal potassium wasting nor hyperaldosteronism could be explained as a consequence of a gradient restriction on renal H(+) - Na(+) exchange because the urinary pH remained greater than, or approximately equal to, the normal arterial pH or considerably greater than the minimal urinary pH attained during acidosis. The findings provide no support for the traditional view that renal potassium wasting in either classic RTA or RTA associated with the Fanconi syndrome is predictably corrected solely by sustained correction of acidosis with alkali therapy.
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PMID:Renal potassium wasting in renal tubular acidosis (RTA): its occurrence in types 1 and 2 RTA despite sustained correction of systemic acidosis. 510 85

The kidney is one of the organs susceptible to heavy metal intoxication. The total body burden and "saturation" level in renal tissue are important limiting factors to the onset of renal injuries. Acute or chronic exposure to many of heavy metals can induce renal tubulointerstitial injuries, including acute tubular necrosis, chronic tubulointerstitial nephritis, Fanconi syndrome, renal tubular acidosis, and renal tubular dysfunction without morphological changes. Chronic cadmium intoxication can cause irreversible Fanconi syndrome with chronic tubulointerstitial nephritis. Both urinary low-molecular weight protein excretion and urinary cadmium excretion (greater than 200-400 ppm) are the most reliable earlier markers of tubulointerstitial injury in chronic cadmium intoxication. The role of metallothionein is central to an understanding of cadmium-induced nephropathy. Acute lead intoxication in children can cause reversible Fanconi syndrome. Hypertension, hyperuricemia, and elevated serum creatinine, without Fanconi syndrome, are clinical manifestations of chronic lead exposure in adults. Nuclear inclusion body in proximal tubular cell is characteristic. Chronic exposure to inorganic germanium can cause chronic renal failure without urinary abnormalities, due to tubular degeneration and interstitial fibrosis, mainly in the thick ascending limb of Henle and distal tubulus.
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PMID:[Tubulointerstitial injuries in heavy metal intoxications]. 756 49

Actuarial five-year patient survivals after pediatric orthotopic liver transplantation (OLT) of 75 to 80% are now commonplace. However, renal dysfunction after pediatric OLT remains a serious complication and maybe broadly divided into four categories. The first is pre-existing renal disease in association with liver disease. This includes tyrosinemia with Fanconi syndrome, congenital cystic disease of the liver with associated polycystic disease of the kidney, Alagille's syndrome and primary hyperoxaluria. Second is hepatorenal syndrome. Resolution is dependent on successful OLT, although short-term dialysis may be required. Children with renal failure prior to transplantation have a significantly increased mortality. Third is peri- and early post-transplant renal impairment. The four major influences on early renal function after OLT are: (i) pretransplant renal function; (ii) early liver graft function; (iii) induction therapy with cyclosporine and tacrolimus; (iv) use of other nephrotoxic drugs. Fourth is long-term nephrotoxicity of cyclosporine and tacrolimus (FK-506). Both of these essential immunosuppressives carry the risk of long-term irreversible toxicity. In one study children, treated with cyclosporine, surviving > one year after OLT, 73% had a true GFR < 77 ml/min/1.73 m2. Children treated for > or = 24 months had a significantly lower GFR than those treated from 12 to 24 months. Half the children with a GFR < or = 50 ml/min/1.73 m2 had hypertension. Another study showed that 46% of pediatric OLT patients had a > or = 20% decrease in GFR over two to four years. FK-506 nephrotoxicity is comparable to that of cyclosporine. In a randomized control trial comparing FK-506 and cyclosporine, there was a 52% decrease in GFR over the first year in the FK-506 group, which was not significantly different to that of the cyclosporine group. In 60% of patients converted from cyclosporine to FK-506 one study showed a 50% or more drop in GFR. Both FK-506 and cyclosporine are associated with hypertension, hyperkalemia, hypomagnesemia and metabolic acidosis. In conclusion, the prognosis for long-term renal function in pediatric OLT patients is as yet unknown. Debate continues as to whether the impairment is static or progressive. Long-term follow-up studies of GFR are essential.
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PMID:Renal function in pediatric liver transplant patients. 877 Sep 96

A 2-year-old male patient was evaluated for Fanconi syndrome with hypertension and failure to thrive. Renal biopsy revealed autoimmune interstitial nephritis with membranous nephropathy. The patient developed autoimmune hemolytic anemia and intractable diarrhea with villous atrophy of the jejunum. He progressed to end-stage renal disease and was transplanted without recurrent disease. Immune work-up done prior to immunosuppressive therapy showed marked elevation of IgE. Studies of T lymphocyte cytokine production showed normal production of interleukin-4 but depressed levels of interferon-gamma. The simultaneous occurrence of autoimmune interstitial nephritis and membranous nephropathy in a young male represents a unique syndrome. Abnormalities of T lymphocyte subpopulations and their cytokines may be involved in the pathogenesis of this disorder.
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PMID:The syndrome of autoimmune interstitial nephritis and membranous nephropathy. 943 46

To determine the incidence of renal functional abnormalities after lead poisoning, we evaluated the parameters of renal tubular function in 134 children and young adults, 8-13 years after chelation therapy for severe lead poisoning. There was no evidence of hypertension or reduced kidney function as assessed by serum creatinine (Cr) concentrations. Urinary alpha-amino nitrogen (Uaan) concentrations were significantly increased compared with 19 healthy age-matched controls. Ninety-four children (70%) had aminoaciduria (Uaan/Cr >0.23). Urinary glucose excretion was also significantly higher than that of 2 historical controls. Thirty-two children (24%) had glycosuria (>125 mg/24 h). Fractional excretion of phosphate was normal in all children. We conclude that a partial Fanconi syndrome can persist up to 13 years after childhood lead poisoning.
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PMID:Aminoaciduria and glycosuria following severe childhood lead poisoning. 963 41

The use of herbal therapy has increased dramatically in past years and may lead to renal injury or various toxic insults, especially in renal patients. In most countries, herbal products are not regulated as medicines. Herbal poisoning may be secondary to the presence of undisclosed drugs or heavy metals, interaction with the pharmacokinetic profile of concomitantly administered drugs, or association with a misidentified herbal species. Various renal syndromes were reported after the use of medicinal plants, including tubular necrosis, acute interstitial nephritis, Fanconi's syndrome, hypokalemia or hyperkalemia, hypertension, papillary necrosis, chronic interstitial nephritis, nephrolithiasis, urinary retention, and cancer of the urinary tract. It seems critical that caregivers be aware of the potential risk of such often underreported therapy and carefully question their patients about their use of this popular branch of alternative medicine.
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PMID:Herbs and the kidney. 1521 32

In the developing world, up to 80% of the population uses traditional medicine for primary health care. In industrialized countries, adaptations of traditional medicine, termed "complementary" or "alternative" medicine (CAM), are used by a growing number of patients for preventive or palliative care. However, alternative medicine (AM) may be an important risk for the development of acute and chronic kidney injury because of several factors: nonconventional preparations rarely meet the required essential standards of consistency in composition and biological activity; many of these products contain undisclosed over-the-counter or prescription drugs or can be adulterated with hormones and glandular extracts; herbal preparations can be contaminated by pesticides and heavy metals; and because of errors in plant identification and confusing terminology, opportunities for mistakes and deliberate substitution can occur. Furthermore, there is a lack of reports of adverse events and drug interactions because of a lack of professional surveillance, and specific data on systemic and kidney toxicity are not easily available. Kidney injury/kidney syndromes caused by AM consist of acute tubular necrosis/toxicity (eg, Fanconi's syndrome), acute interstitial nephritis, papillary necrosis, hypertension, kidney stones, urinary retention, chronic tubulointerstitial nephritis with fibrosis, urinary tract carcinoma, and acute rejection of the kidney transplant. To improve the care for patients using AM, extension of physicians' knowledge about its possible hazards and toxicity is essential. This review deals with acute and chronic kidney toxicity caused by animal-, plant-, and mineral-based, nonconventional medicine and kidney failure caused by drug interactions with AM.
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PMID:Kidney injury from alternative medicines. 1601 Jun 41


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