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PubMed2004

Tubulointerstitial nephritis and uveitis in monozygotic twin boys.

We describe monozygotic male twins who developed tubulointerstitial nephritis and uveitis (TINU) almost 2 years apart. They presented with non-specific symptoms and were noted to have glycosuria and renal impairment. Both children have uveitis. One had biopsy-proven interstitial nephritis and the other had biochemical evidence of transient tubular dysfunction. While the renal parameters improved, they are still under treatment for uveitis. The occurrence of TINU in identical twins at an interval of just under 2 years supports a strong genetic element in the aetiology of this syndrome. We believe this is the first report of male twins with TINU.

Child↗

PubMed2004

Hyponatremic-hypertensive syndrome with extensive and reversible renal defects.

Two young children with renal artery stenosis and severe hypertension who presented with the so-called hyponatremic-hypertensive syndrome (HHS), with marked urine and solute loss during the acute phase, are described. Both children also presented with severe high molecular proteinuria, glycosuria, and hypercalciuria, only the first symptom having prompt remission after normalization of blood pressure. In children with renal artery stenosis, HHS is associated with severe proteinuria due to hyperfiltration and more extensive tubular functional alterations. Hyponatremia and acute tubulopathy may mask the presenting clinical picture of renal artery stenosis.

Child, Preschool↗

PubMed2006

Mild course of Puumala nephropathy in children in an area with sporadic occurrence Hantavirus infection.

The first three children with Puumala virus nephropathy diagnosis in the Czech Republic are reported on. A boy and two girls were admitted with symptoms of interstitial nephritis. The medical history in all children revealed flu-like symptoms. All patients were mildly pyrexial and had elevated erythrocytes sedimentation rate, C-reactive protein and low hemoglobin levels. Serum creatinine levels were elevated and proteinuria exceeded 700 mg/L in all children. Tubular proteinuria, glycosuria, high urinary N-acetyl-beta-D-glucosaminidase levels and alpha-1-microglobulin levels confirmed the tubular lesion. Renal biopsies revealed a uniform pattern and showed non-purulent interstitial nephritis in all patients. Puumala virus antigen antibodies were detected in the plasma. All patients were treated with steroids and urine abnormalities and renal function returned to normal within 4 weeks. Hantavirus infection should be considered as one of possible causes of interstitial nephritis with decreased GFR in children even in areas with a low incidence of this infection.

Adolescent↗

PubMed1997

Renal involvement in the Laurence-Moon-Bardet-Biedl syndrome: report of five cases.

We report five patients with Laurence-Moon-Bardet-Biedl syndrome (LMBBS) who had renal involvement. Intravenous pyelography showed bilateral or unilateral calyceal clubbing and blunting in all patients. In addition, one patient had a parapelvic cyst in the left kidney and another had bilateral lobulated renal outlines of the fetal type. One patient had a urinary concentrating defect and two patients showed increased fractional sodium excretion. Estimated tubular phosphate reabsorption values were in normal limits in all of five patients. No patient had a urine acidification defect, proteinuria, glycosuria, or hyperaminoaciduria. One patient died from end-stage renal failure. The remaining four patients had normal serum creatinine values and estimated creatinine clearances. 99mTechnetium-diethylenetriamine pentaacetate renal scanning showed prolonged and delayed concentration and delayed excretion in three of the four patients who survived. A focal scar was determined on the left kidney of one of four patients by 99mtechnetium-dimercaptosuccinic acid renal scanning. All LMBBS cases with or without renal symptoms should be routinely evaluated for renal abnormalities. Renal scanning is a valuable method, especially for determining the renal involvement in the early stage of disease.

Adolescent↗

PubMed1998

Serum 1,5-anhydro-D-glucitol levels in liver cirrhosis.

We studied the serum 1,5-anhydro-D-glucitol (AG) levels, a marker of glycemic control, in liver cirrhotic patients who had no evidence of glycosuria in 24-h urine samples in order to clarify the effects of impaired liver function on serum AG metabolism. We showed first that serum AG concentrations were significantly lower in cirrhotic patients than in age- and sex-matched healthy controls (17.6+/-1.6 vs 26.3+/-1.7 microg/ml, P<0.05). Moreover, serum AG levels were found to be positively correlated with both serum cholinesterase and albumin levels. The observations indicate that serum AG levels were decreased in liver cirrhosis, especially in cases of severely reduced hepatic functions, suggesting the possibility of altered AG synthesis in liver cirrhosis.

Cholinesterases↗

PubMed2004

Adult onset Fanconi syndrome: extensive tubulo-interstitial lesions and glomerulopathy in the early stage of Chinese herbs nephropathy.

A 33-year-old woman was transferred to our hospital with a 5-month history of taking Chinese herbal medicine containing aristolochic acid. She presented with metabolic acidosis, severe anemia, hypophosphatemia and uric aciduria, and generalized aminoaciduria and glycosuria, features which were consistent with the clinical manifestations of Fanconi syndrome. Renal biopsy was performed when her plasma creatinine was 0.7 mg/dl and creatinine clearance was 46 ml/min per 1.73 m(2). The renal specimen showed extensive interstitial edema with focal fibrosis, tubular atrophy, and focal glomerulopathy, which suggested the presence of glomerular endothelial damage or glomerular ischemia. Although steroid therapy ameliorated the plasma electrolyte levels, renal failure progressed, and hemodialysis therapy was initiated approximately 18 months after the time of renal biopsy. This patient demonstrated the early renal lesions of Chinese herbs nephropathy in association with various clinical manifestations. The characteristic glomerulopathy found in the present patient is considered to be an additional renal lesion, leading to the renal failure.

Adult↗

PubMed1979

Tumorous phosphaturic osteomalacia. Report of a case associated with multiple hemangiomas of bone.

A case of osteomalacia associated with hypophosphatemia, decreased tubular reabsorption of phosphorus, hyperphosphaturia and renal glycosuria with associated bone pain and myopathy is presented. The patient was found to have multiple osteolytic lesions of bone which, on biopsy, proved to be sclerosing hemangiomas of bone. Treatment with oral phosphate and vitamin D effected a diminution in his symptoms of bone pain and muscular weakness. The literature on hypophosphatemic phosphaturic osteomalacia associated with mesenchymal tumors is reviewed. It has been suggested that certain mesenchymal tumors elaborate a yet to be identified humoral substance which decreased synthesis of 1 alpha, 25-dihydroxycholecalciferol causing decreased tubular reabsorption of phosphorus, hyperphosphaturia, hypophosphatemic osteomalacia and hypophosphatemic myopathy.

Adult↗

PubMed1981

Renal involvement in Refsum's disease.

Renal hemodynamic and tubular functions were measured in a patient with Refsum's disease before and after 12 weeks of twice-weekly plasmaphereses. Percutaneous renal biopsy was performed before initiation of plasmapheresis. These studies were performed to (1) define the nature of the renal lesions and the effects of phytanic acid accumulation on renal functions, and (2) assess the effects of lowering the plasma phytanic acid level on renal functions. The patient, a 39 year old woman, had lipiduria, glycosuria, cylindruria, minimal proteinuria and mild azotemia initially. Renal lesions consist of extensive vacuolization and mitochondrial changes of the tubular epithelial cells, vacuolization of the visceral epithelial cells of the glomeruli, and slight to moderate mesangial sclerosis. The impaired renal hemodynamic function and various tubular functions improved following plasmaphereses associated with reduction of plasma phytanic acid. Over-all clinical improvement was also evident.

Adult↗

PubMed1982

Disorders of proximal nephron function.

The proximal nephron is responsible for reabsorbing 80 to 99 percent of several filtered solutes, including amino acids, glucose and bicarbonate. Separate, high-affinity sodium co-transport mechanisms are used. Increasing luminal concentration of each of these solutes stimulates its active transcellular reabsorption until there is saturation. Slightly less than half of the filtered chloride is reabsorbed, partly by passive mechanisms that are linked to the reabsorption of organic solutes and bicarbonate, as well as by less well defined independent cellular and/or paracellular mechanisms that appear to be sensitive to transepithelial osmotic pressure gradients. Proximal tubule reabsorption is isosmotic and isonatric, and about 50 to 60 percent of the filtered sodium and water in reabsorbed. Disorders or proximal nephron function include conditions in which luminal, cellular and/or peritubular factors affecting reabsorption are altered. Clinical disorders caused by modification of the luminal reabsorptive determinants include conditions in which tubular flow rate is increased or luminal composition is altered, as when non-reabsorbable solutes (mannitol) are filtered or when reabsorbable solutes (glucose) are filtered in concentrations exceeding their tubular transport capacity. Other disorders occur due to loss of affinity or capacity of the cellular active transport systems for specific solutes, such as amino acids (renal aminoacidurias), glucose (renal glycosurias) and bicarbonate (proximal renal tubular acidosis), or for all solutes (Fanconi syndrome). Finally, disorders due to changes in the peritubular factors affecting reabsorption include states of altered peritubular Starling forces or pH, which modify sodium chloride or sodium bicarbonate reabsorption, respectively.

Absorption↗

PubMed1985

Fanconi syndrome associated with a non-ossifying fibroma of bone.

A 20-year-old man presenting with osteomalacia was found to have the Fanconi syndrome, as evidenced by hypophosphatemia with hyperphosphaturia, glycosuria in the presence of normoglycemia, and generalized aminoaciduria. After removal of a non-ossifying fibroma of the left tibia, the renal tubular abnormalities promptly resolved with subsequent healing of the osteomalacia. A humoral factor released from the tumor may have caused the disorder in proximal renal tubular cell transport.

Adult↗

PubMed1988

Large variations of sucrose in constant carbohydrate diets in type II diabetes.

Several studies show that sucrose does not aggravate hyperglycemia in type II diabetes mellitus, but sucrose is still restricted in dietary recommendations. Since sucrose in high carbohydrate diets elevates fasting triglyceride levels, the effects of sucrose were evaluated in diets with fixed carbohydrate levels. Eighteen diabetic volunteers receiving no medication were given weight maintenance diets with 50 percent carbohydrate, 35 percent fat, 15 percent protein, and 120 g of sucrose for 10 days as inpatients. They were then randomly assigned diets of similar composition with either 220 g of sucrose (high sucrose diet) or less than 3 g of sucrose daily (complex carbohydrate [CHO] diet) for one additional month. There were no differences in fasting, one-, two-, and three-hour post-lunch serum glucose levels; 24-hour glycosuria; glycohemoglobin levels; fasting and postprandial serum triglyceride levels, or fasting high-density lipoprotein-cholesterol levels. Twelve patients with preexisting higher triglyceridemia had similar trends, but the postprandial triglyceride levels were lower in the high sucrose diet group of this subset (p less than 0.05 in the third week). Postprandial serum insulin levels declined in the second week on the complex CHO diet. More than 75-fold difference in sucrose intake with constant carbohydrate and fat did not affect glycemic or triglyceridemic control in type II diabetic patients. The reported high sucrose-carbohydrate-induced rise in fasting triglyceridemia was not present when a diet high in sucrose was given without changing total carbohydrate.

Blood Glucose↗

PubMed1975

Effect of abnormal glucose tolerance in pregnancy on infant mortality rate and morbidity. A prospective study.

Ninety-five pregnant women, not previously known to have diabetes but suspected of being at risk for the disease because of obesity, glycosuria, family history, or obstetric history, underwent oral and intravenous glucose tolerance tests in the last trimester of pregnancy. Several methods were used to categorize the degree of abnormality, but none was of value in predicting pregnancy outcome. Perinatal mortality and malformation rates in the offspring of these women were no greater than those of the over-all infant population at this Center and were much lower than those in infants born to women with overt diabetes. Causes of infant morbidity were not increased, with the exception of overweight babies, hypoglycemia, and hypocalcemia. Umbilical vein glucose level correlated significantly with the mothers' blood glucose at the time of delivery. Cord insulin level correlated with infant birth weight and with University Group Diabetes Program number. Birth weight correlated with the degree of the mothers' obesity. It was concluded the documentation of the degree of glucose intolerance in the mother is of little value in predicting fetal outcome but may indicate infants at risk for hypoglycemia and hypocalcemia.

Birth Weight↗

PubMed1978

Acid glycohydrolase in Chinese hamster with spontaneous diabetes. I. Depressed levels of renal alpha-galactosidase and beta-galactosidase.

The activites of alpha-and Beta-galactosidases (alpha-D-galactoside galactohydrolase, EC 3.2.1.22; beta-D-galactoside galactohydrolase, EC 3.2.1.23) were significantly lower in the kidneys of diabetic XA line than those in the nondiabetic M line Chinese hamsters. The depression of these enzymes was found only in the kidney but not in liver, spleen, hind leg muscle, cheek pouch or spinal cord. In young XA animals before onset of glycosuria, renal alpha-galactosidase level was similar to that in age-matched M animals; whereas, their renal beta-galactosidase activity was about 90% of those in the M animals. Partial purification and separation of these enzymes were achieved by chromatography on DEAE-Sepharose CL-6B columns. beta-galactosidase was separated into two isozymes and depression of activity in the XA kidneys was evident in both. alpha-galactosidase was recovered in a single peak. The pH optima of these enzymes from XA and M animals were identical. With p-nitrophenyl glycosides as substrates, the Michaelis constants of these enzymes were also the same of XA and M animals. Molecular weight estimation by gel filtration on Sepharose 6B yielded similar results between M and XA samples: 2.4-10(5) for alpha-galactosidase and 1.6.10(5) and 1.9.10(5) for beta-galactosidase isozymes. The data suggest that the diabetic animals had lower concentrations of alpha-and beta-galactosidase in their kidneys, probably as a consequence of hyperglycemia.

Animals↗

PubMed1981

Hyperzincuria in insulin treated diabetes mellitus--its relation to glucose homeostasis and insulin administration.

In order to elucidate some pathogenic factors of diabetic hyperzincuria we studied 60 adult insulin treated diabetic out-patients (40 males and 20 females), all with normal serum creatinine concentrations and absence of proteinuria during a 24-h period. Diabetic males and females both had significantly (p less than 0.01) increased zinc excretion rates (1.14 +/- 0.06 (S.E.M.) mumol/mmol creatinine and 1.37 +/- 0.10 mumol/mmol creatinine) compared with normal males and females (0.55 +/- 0.06 and 0.48 +/- 0.08, respectively). The urinary zinc excretion rate correlated positively with the degree of glycosuria (r = 0.36, p less than 0.01), but was not associated with the duration of the disease. However, serum zinc levels gave no evidence of a state of zinc depletion in these patients. It was calculated that zinc originating from a diabetic bone loss and the exogenous insulin administration accounted for only a small part of the hyperzincuria. Compensatory hyperabsorption and/or increased zinc content in the diabetic diet may therefore serve to explain the lack of zinc depletion in the presence of hyperzincuria.

Adult↗

PubMed1982

Hyponatremia and hyperkalemia in relation to hyperglycemia in insulin-treated diabetic out-patients.

Interrelations between glucose and electrolyte homeostasis were evaluated in 193 insulin-treated diabetic out-patients. All had normal serum creatinine and were studied during their everyday metabolic control. Although the patients were selected to be without proteinuria and ketonuria, they exhibited wide ranges of blood glucose values (2.5-29.5 mmol/l) and urine glucose excretions (0-301 mmol/mmol creatinine). Patients with blood glucose values within 2.5-10 mmol/l (n = 80) had entirely normal levels of serum sodium (140.6 +/- 2.7 (SD) versus 141.0 +/- 2.6 mmol/l) and potassium (4.35 +/- 0.38 versus 4.40 +/- 0.38 mmol/l) as compared with normals (n = 371). In contrast, diabetics with higher blood glucose concentrations (n = 113) showed hyponatremia (137.7 +/- 2.6 mmol/l, p less than 0.001) and a moderate increase of serum potassium (4.60 +/- 0.39 mmol/l, p less than 0.001). On stratification into classes of blood glucose, serum sodium declined from 142 to 135 mmol/l (r = -0.61, p less than 0.001), whereas serum potassium rose from 4.33 to 4.87 mmol/l (r = 0.37, p less than 0.001). Despite these reciprocal changes the urinary excretion rates relative to creatinine of sodium potassium and water rose with rising degrees of glycosuria (r = 0.24, p less than 0.001; r = 0.28, p less than 0.001; and r = 0.63, p less than 0.001, respectively). The decline in serum sodium represents a well-known osmoregulatory response to hyperglycemia. However, the rising level of serum potassium in virtual absence of renal failure and ketonuria suggests an abnormality in potassium homeostasis. Diabetic dysregulation, or rather insulin deficiency may be its cause.

Cross-Sectional Studies↗

PubMed1985

Intraportal autotransplantation of cryopreserved porcine islets of Langerhans.

Mechanically prepared isolated islets of Langerhans were cryopreserved in liquid nitrogen for a period of 4 days. Intraportal autotransplantation studies were performed on two groups of six pigs rendered diabetic by total pancreatectomy (group 2) or by partial pancreatectomy combined with streptozotocin (group 4) and compared with two control groups (groups 1 and 3, respectively). The pigs were assessed for survival, weight gain, glycosuria, polyuria, systemic blood sugar and insulin, and, in selected pigs, intravenous glucose tolerance tests. Results showed that partial pancreatectomy with streptozotocin was the better tolerated experimental diabetes. Variable control of hyperglycemia was obtained over an experimental period of 3 months. Random blood glucose returned to normal in one of six pigs in the totally pancreatectomized group and three of six pigs in the partial pancreatectomy and streptozotocin group. Despite these normal circulating glucose levels, imperfect glucose homeostasis was achieved as shown by the response to glucose tolerance testing. These results report blood glucose control after cryopreserved islet autotransplants in diabetic pigs but further study is still necessary to achieve consistency.

Animals↗

PubMed1983

Impaired renal function in diabetic chimpanzees (Pan troglodytes).

Studies were conducted to assess the renal functional state in two recently discovered diabetic chimpanzees. Both were nonobese, adult female animals with the non-insulin-dependent form of impaired glucose tolerance, analogous to the Type II or nonobese, maturity-onset diabetes of humans. Both animals displayed moderate-to-heavy proteinuria and glycosuria in response to intravenous administration of glucose or tolbutamide. Chimpanzee number 333, but not number 1037, had fasting proteinuria and chronic hypertension. Renal function studies, using the inulin clearance method, demonstrated significantly decreased glomerular filtration rates and elevated rates of sodium excretion for both animals. The rate of chloride excretion was also elevated in animal number 1037, but potassium excretion was apparently unaffected in both animals. Abnormal serum biochemical parameters demonstrated for chimpanzee number 333 included elevations in calcium, magnesium, creatinine, urea nitrogen, and uric acid; animal number 1037 had only an elevated serum creatinine. Results are consistent with the occurrence of renal disease similar to the nephropathy that develops in human diabetics. The difference in severity of renal impairment in the two chimpanzees is possibly related to differences in duration and severity of impaired glucose tolerance. A progression of both diabetic and renal disorders is most probable.

Animals↗

PubMed1995

Diabetes in pregnancy.

OBJECTIVE: To determine whether there is an association between the level of glycemic control and perinatal complications in pregnant diabetic patients. METHODS: Two hundred sixty confirmed cases of pre-existing diabetes, gestational diabetes and impaired glucose tolerance were analyzed to assess risk factors, modality of treatment, level of blood sugar control and effect on perinatal morbidity and mortality. RESULTS: Risk factors for the development of diabetes included age ( > 25 years), East Indian ethnic origin, glycosuria, and a history of diabetes in a first-degree relative. Treatment consisted of diet alone or in combination with soluble insulin. There is a marked increase in perinatal mortality and maternal morbidity if normoglycemia is not maintained. CONCLUSIONS: A greater emphasis must be placed on the detection of diabetes in pregnancy and effective treatment should be instituted as early as possible to achieve normoglycemia if associated complications are to be reduced.

Adolescent↗