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PubMed1992

Kidney function in very low birth weight infants with furosemide-related renal calcifications at ages 1 to 2 years.

To determine whether long-term renal sequelae follow the use of furosemide in preterm infants, we evaluated renal function in 27 former very low birth weight infants (less than 1500 gm) at 1 to 2 years of age. Patients were classified into three groups on the basis of status at the time of discharge from the hospital: group 1 (n = 7) had no furosemide treatment or renal calcifications, group 2 (n = 10) had furosemide therapy but no calcifications, and group 3 (n = 10) had furosemide therapy with renal calcifications. Renal ultrasonography at the time of the study demonstrated resolution of the calcifications in six patients in group 3. No differences in renal function were observed between groups 1 and 2. Creatinine clearance (mean +/- SEM) in group 3 (83.6 +/- 7.8 ml/min per 1.73 m2) was significantly lower than clearance in groups 1 and 2 (103.2 +/- 6.5 and 109.1 +/- 5.1, respectively; p less than 0.05). Children in group 3 had significantly higher urinary calcium/creatinine ratios and fractional excretion of sodium and lower tubular reabsorption of phosphate than children in the two other groups had. Urine-blood difference in carbon dioxide tension after oral acetazolamide load, which indicates the ability of the distal tubule to secrete hydrogen ions, was 8.4 +/- 3.4 mm Hg in group 3, significantly lower than values in groups 1 and 2 (22.6 +/- 3.1 and 28.0 +/- 4.3 mm Hg, respectively, p less than 0.05). Within group 3 the four children with persistent renal calcifications had significantly lower urine-blood carbon dioxide tension differences than did those with resolution of calcifications (p = 0.02). We conclude that furosemide-related renal calcifications in very low birth weight infants may lead to glomerular and tubular dysfunction; further long-term follow-up of this population is recommended.

Absorption↗
PubMed1988

[Comparison of captopril with enalapril in the therapy of heart failure: effect on hemodynamics and kidney function].

24 patients with severe heart failure (NYHA III) were randomly assigned to an additional therapy with captopril or enalapril. The mean daily dose of captopril was 56 +/- 2 mg and of enalapril, 9.6 +/- 0.9 mg. After a mean of 9 days, the influence of both inhibitors of the angiotensin converting enzyme (ACE-inhibitors) on hemodynamics and renal function was evaluated. The mean arterial pressure in the group treated with captopril (group A) fell by 11 +/- 2 mm Hg (p less than 0.001), with enalapril (group B) by 13 +/- 3 mm Hg (p less than 0.01), the difference between the groups not being significant. Heart rate decreased in both groups to a similar degree. The change was significant only in the patients treated with enalapril (13 +/- 4/min; p less than 0.05 vs. 11 +/- 5/min in group A). Stroke volume index increased by 10 +/- 2 ml/m2 in group A vs. 12 +/- 2 ml/m2 in group B; both increases were highly significant (p less than 0.001). Mean decreases in pulmonary artery and right atrial pressure were comparable in both groups. The hemodynamic improvement was not different with both ACE-inhibitors. Serum sodium and potassium before therapy were 137 +/- 1 mmol/l and 4.1 +/- 0.2 mmol/l in group A and 139 +/- 1 mmol/l and 3.8 +/- 0.1 mmol/l in group B and serum creatinine was 1.2 +/- 0.1 mg/dl in both groups. Neither serum electrolytes nor serum creatinin were changed significantly by therapy with captopril or enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Serum cystatin C is superior to serum creatinine as a marker of kidney function: a meta-analysis.

BACKGROUND: Serum cystatin C (Cys C) has been proposed as a simple, accurate, and rapid endogenous marker of glomerular filtration rate (GFR) in research and clinical practice. However, there are conflicting reports regarding the superiority of Cys C over serum creatinine (Cr), with a few studies suggesting no significant difference. METHODS: We performed a meta-analysis of available data from various studies to compare the accuracy of Cys C and Cr in relation to a reference standard of GFR. A bibliographic search showed 46 articles until December 31, 2001. We also retrieved data from eight other studies presented and published in abstract form. RESULTS: The overall correlation coefficient for the reciprocal of serum Cys C (r = 0.816; 95% confidence interval [CI], 0.804 to 0.826) was superior to that of the reciprocal of serum Cr (r = 0.742; 95% CI, 0.726 to 0.758; P < 0.001). Similarly, receiver operating characteristic (ROC)-plot area under the curve (AUC) values for 1/Cys C had greater identity with the reference test for GFR (mean ROC-plot AUC for Cys C, 0.926; 95% CI, 0.892 to 0.960) than ROC-plot AUC values for 1/Cr (mean ROC-plot AUC for serum Cr, 0.837; 95% CI, 0.796 to 0.878; P < 0.001). Immunonephelometric methods of Cys C assay produced significantly greater correlations than other assay methods (r = 0.846 versus r = 0.784; P < 0.001). CONCLUSION: In this meta-analysis using currently available data, serum Cys C is clearly superior to serum Cr as a marker of GFR measured by correlation or mean ROC-plot AUC.

Biomarkers↗
PubMed1986

Renal water excretion before and after remission of nephrotic syndrome: relationship between free water clearance and kidney function, arginine vasopressin, angiotensin II and aldosterone in plasma before and after oral water loading.

An oral water load of 20 ml/kg body wt. was given to eight patients with nephrotic syndrome before and after remission of the syndrome, and to 13 healthy control subjects. Urine volume (D), free water clearance (C water), plasma concentrations of arginine vasopressin (AVP), angiotensin II (ANG II) and aldosterone (Aldo), were determined before and three times during the first 4 h after loading. D and C water increased to a significantly lower level (P less than 0.01) after water loading in patients with nephrotic syndrome than in control subjects, but D and C water were normal after remission of the syndrome. The maximum increase in C water (delta C water max.) was 1.07 ml/min (median) before remission and 7.93 ml/min after, compared with 8.01 ml/min in the control group. Creatinine clearance (Ccr) increased significantly after remission (63 ml/min to 88 ml/min, P less than 0.01), and the fractional excretion of sodium was enhanced. AVP was higher in the nephrotic syndrome both before (2.9 pmol/l) and after remission (2.9 pmol/l) compared with the control group (1.8 pmol/l). ANG II and Aldo did not change after remission and remained at the same level as in the control group. The elevation in delta C water max. after remission was accompanied by an increase in Ccr in all patients and delta C water max. and Ccr were significantly correlated (rho = 0.600, n = 16, P less than 0.05). No relationship was found between the change in delta C water max. and ANG II and Aldo.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1985

Comparative effects of indomethacin on hepatic enzymes and histology and on serum indices of liver and kidney function in the rat.

The effects of high-dose indomethacin (three daily dose, 8.5 mg/kg ip) on pathology and histology, on serum and urine biochemistry, and on various hepatic enzyme activities were studied in rats. Hepatic cytochrome P-450 and aminopyrine N-demethylase were decreased by 52-62%, but glucuronyl transferase fell by only 22%. Hepatic glucose-6-phosphatase, aryl esterase, 6-phosphogluconate dehydrogenase and sulphotransferase remained unchanged, while glucose-6-phosphate dehydrogenase increased by 29%. There were no widespread changes in hepatic and renal pathology or histology, but noteworthy was a mild, focal, centrilobular hepatic response. By contrast, there were severe intestinal lesions: the effects on hepatic enzymes might have been partly a consequence of the intestinal damage. There was a reversible uraemia and significant decreases (20-40% below normal) in both serum albumin and protein, while serum levels of creatinine and aspartate-amino-transferase activity remained constant. A reversible N-acetyl-beta-D-glucoseaminidase (NAG) enzymuria occurred (300% above normal), but no significant proteinuria (less than 300 mg/l). Administration of 16, 16-dimethylprostaglandin F2 alpha(0.5 mg/kg iv) concomitantly with the indomethacin greatly ameliorated the intestinal lesions and prevented the decreases in hepatic drug-metabolizing enzymes. Concomitant 16,16-dimethylprostaglandin F2 alpha did not, however, influence the indomethacin-induced decreases in serum protein, albumin or NAG-enzymuria. It was concluded that indomethacin had a highly selective effect causing a decrease in hepatic cytochrome P-450, which was not accompanied by severe damage to hepatocyte structure.

Acetylglucosaminidase↗
PubMed1991

[Enalapril versus captopril in heart failure--effect on blood pressure and kidney function].

In 33 patients with heart failure (NYHA II-III) the 24-h blood pressure was examined during the titration of two ACE-inhibitors. Blood pressure was measured by the oscillometric method using the blood pressure monitor 90202 from SpaceLabs, Inc.. All patients received an additional therapy either with captopril (group A, n = 17) or enalapril (group B, n = 16) in random order. Serum-electrolytes, serum- and urine-creatinine, and plasma-renin- activity were measured before and during therapy with both ACE-inhibitors. 24-h blood pressure measurements were taken before and on the first and fifth days of the treatment with ACE-inhibitors. Neither group was different with respect to the degree of heart failure, the concomitant medication, and the 24-h profiles of blood pressure and heart rate. The mean initial dose of captopril was 9.2 +/- 1.2 mg which was titrated to a mean daily dose of 40.7 +/- 3.3 mg given three-times daily. Each patient of group B received an initial dose of 2.5 mg enalapril and a mean maintenance dose of 8.4 +/- 0.9 mg once daily. The first dose effect on blood pressure was similar with captopril and enalapril with a maximal decrease of systolic and diastolic blood pressure of 8/8 mmHg (after 1 h) in group A and of 9/7 mmHg (after 4 h) in group B. The 24-h blood pressure values on day 5 were consistently below the pretreatment values (p less than 0.005) but heart rate was not significantly affected by either ACE-inhibitor. Neither group differed significantly during ACE-inhibition in their 24-h blood pressure and heart rate profiles.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMedDate not supplied

[Characteristics of the kidney functional state after a single dose of thyroxine in white rats].

A 50 mcg/100 g b.w. single dose of thyroxine was injected to non-inbred white rat males with body mass 140-180 g in conditions of 5% water and osmotic (3% solution of sodium chloride) load, then renal function was studied. This injection reduced creatinine clearance and phosphate excretion, raised nitrate and protein excretion. The kidney of the hyperthyroid animals retains ability to increase creatinine clearance in response to osmotic load. Thus, the above model demonstrates that in the absence of thyroxine renal toxicity it changes homeostatic renal functions both at the vascular-glomerular and tubular levels.

Animals↗
PubMed2000

Effect of nebivolol, a novel beta 1-selective adrenoceptor antagonist with vasodilating properties, on kidney function.

Nebivolol (CAS 99200-09-6) is a novel beta 1-selective adrenoceptor antagonist which possesses vasodilating properties and lowers systemic vascular resistance in dogs and humans, presumably by a nitric oxide-related mechanism. In the present study, clearance techniques were applied to anaesthetized male Sprague Dawley rats, and the effects of nebivolol on renal hemodynamics (glomerular filtration rate and renal plasma flow), on urinary excretion of sodium, chloride and potassium, on renal NO-excretion, and on plasma renin activity were studied. Nebivolol doses ranging from 0.1 to 2 mg/kg i.v. were tested. The results revealed that nebivolol dose-dependently increased glomerular filtration rate, urine flow and urinary excretion of sodium and chloride. Potassium excretion was only inconsistently increased and showed no dose dependency. At a dose of 1 mg/kg, the drug also significantly increased renal plasma flow measured as 3H-PAH (p-aminohippurate) clearance. The effect of nebivolol on the glomerular filtration rate could be abolished by L-NMMA (N6-monomethyl-L-arginine) (1 mg/kg), a non-selective inhibitor of NO-synthase and by iminoethyllysine (1 mg/kg), a relatively selective inhibitor of the inducible NO-synthase, but not by 7-nitroindazole (1 mg/kg), a relatively selective inhibitor of the neuronal NO-synthase isoform. The saluretic effect of nebivolol was diminished by all of the three NO-synthase inhibitors, but could not be completely reversed. At a dose of 2 mg/kg, nebivolol increased renal NO-excretion by 70.7%. This effect could be completely abolished by L-NMMA (1 mg/kg). Plasma renin activity was lowered by nebivolol (2 mg/kg) from 14.6 +/- 1.49 to 6.5 +/- 1.66 ng angiotensin I/ml/h (p < 0.01). The results demonstrate that, in anaesthetized rats, nebivolol exerts significant renal vasodilating effects and increases urinary excretion of fluid and solutes. The actions of nebivolol on renal hemodynamics are assumed to be mediated by a stimulation of the NO-synthase, probably the inducible isoform. Since none of the NO-synthase inhibitors could completely abolish the saluretic effect of nebivolol, an additional mechanism, not related to NO, may be involved in the tubular action of this drug.

Adrenergic beta-1 Receptor Antagonists↗
PubMed2004

Hyperphosphatemia in Chinese peritoneal dialysis patients with and without residual kidney function: what are the implications?

BACKGROUND: Hyperphosphatemia is an important predictor for mortality in hemodialysis patients. This study evaluated significant factors associated with hyperphosphatemia in peritoneal dialysis (PD) patients. METHODS: We estimated residual renal function (RRF), dialysis adequacy, and normalized protein equivalent nitrogen appearance (nPNA), together with simultaneous measurement of serum phosphorus levels in 252 prevalent Chinese continuous ambulatory peritoneal dialysis (CAPD) patients. RESULTS: Average serum phosphorus level was 5.2 +/- 1.5 mg/dL (1.68 +/- 0.48 mmol/L). Serum phosphorus levels were 5.6 mg/dL or greater (> or =1.81 mmol/L) in 44.0% of anuric patients (n = 116) versus 28.7% of patients with RRF (n = 136; P = 0.012). Patients with RRF maintained serum phosphorus levels at or less than the median value (< or =5.1 mg/dL [< or=1.65 mmol/L]), with a total creatinine clearance (CCr) of 72 +/- 25 L/wk/1.73 m2 and nPNA of 0.94 +/- 0.19 g/kg/d in contrast to a total CCr of 63 +/- 22 L/wk/1.73 m2 (P = 0.031) and nPNA of 1.03 +/- 0.22 g/kg/d (P = 0.011) in patients with serum phosphorus levels greater than the median value. Among anuric patients, total CCrs were 46 +/- 9 and 42 +/- 7 L/wk/1.73 m2 (P = 0.005) and nPNA values were 0.89 +/- 0.17 and 0.98 +/- 0.18 g/kg/d (P = 0.010) for patients with serum phosphorus levels at the median value or less and greater than the median value, respectively. Multiple regression analysis showed that residual glomerular filtration, despite an average of less than 2 mL/min/1.73 m2, was independently associated with phosphorus control in PD patients. nPNA, PD CCr or urea clearance, body mass index, and parathyroid hormone level were other important correlates of serum phosphorus levels in patients with and without RRF. CONCLUSION: Hyperphosphatemia is a frequent complication in Chinese CAPD patients. Our study not only shows the importance of RRF in maintaining serum phosphorus levels in PD patients, but also the limitations of PD alone to achieve adequate phosphorus control in anuric patients.

Adult↗
PubMed1988

[The effect of long-term increased protein administration on mineral metabolism and kidney function in the rat. I. Renal and enteral excretion of calcium, magnesium, phosphorus, sulfate and acid].

The influence of continuous imbalanced high protein intake on the metabolism of minerals (calcium, magnesium, phosphorus) and renal function was the subject of a long-term experiment with rats. In the first part of the study particular attention was directed to the contribution of protein-induced endogenous acid production and renal excretion of hydrogen ions and sulphate to the development of hypercalciuria. For 61 weeks 200 male Wistar rats in eight groups were fed isocaloric diets, whose protein contents were increased from 13 to 26 and 40 J% at the expense of carbohydrate intake. The fat content of the diets was 40 J%. In two groups with 13 and 26 J% protein the effect of different kinds of animal protein was also studied, replacing casein by beef. Mineral contents were kept constant in these diets. To examine the excretion mechanisms of calcium and phosphorus especially under conditions of excessive protein intake, the ratio of calcium to phosphorus was varied in three diets with 40 J% protein by increasing both minerals alternatively or together from 0.6 to 1.2%. An increase in dietary protein content from 13 to 26 or 40 J% produced a sustained hypercalciuria and also hypermagnesiuria over a period of more than 400 days (after 58 weeks: 3.3, 5.9, and 6.8 mg calcium/day; 2.2, 3.3, and 3.4 mg magnesium/day; p less than or equal to 0.05). No adaptation to high protein intake occurred. Hypermagnesiuria, which equally hasn't been described before as a result of high protein intake, was accompanied by a reduced fecal excretion of magnesium. With increased protein intake (casein and beef) hypercalciuria and also hypermagnesiuria were positively correlated with an increased formation and renal excretion of hydrogen ions and sulphate, which resulted from protein catabolism. The dietary protein source influenced the extent of hypercalciuria, irrespective of a constant phosphorus intake. Although leading to equal increases in renal total acid and sulphate excretion, beef as the main protein source caused a lower calciuria than casein. High phosphorus intake caused the highest total acid excretion of all groups, but resulted in a reduced hypercalciuria and hypermagnesiuria and counteracted the influence of an increased protein intake.

Acid-Base Equilibrium↗
PubMed1993

[Evaluation criteria for captopril-kidney function scintigraphy using 99mTc-MAG3].

Renal function scintigraphy under ACE inhibition has gained an important role in the diagnosis of renovascular hypertension. Using the radiopharmaceutical 99mTc-MAG3, 54 kidneys with angiographically verified renal artery status were evaluated with respect to the following scintigraphic parameters: intraparenchymal tracer transport, urine drainage, kidney size, and functional side-to-side ratio. In cases of decompensated renal artery stenosis, the typical scan finding using MAG3 was shown to be a distinct parenchymal nuclide retention in combination with a delayed appearance of the radiotracer in the pelvic system. In our patients, the visual impression of the renal sequential scans was superior to quantitative evaluation methods. Using these criteria in 43 patients with suspected renovascular hypertension, sensitivity and specificity were 89% and 88%, respectively. Bilateral positive findings were nonspecific; when excluding them from the study, specificity increased to 100%.

Adult↗
PubMed1987

[Kidney function parameters following ischemia stress using the Euro-Collins solution or the Bretschneider cardioplegic HTK solution].

Protection-methods, for an improvement of ischemic tolerance of the kidney, can be investigated by intraischemic analysis of metabolism and structure. A definite proof for the effectiveness of a protection method is only postischemic function in combination with postischemic structure-regeneration. For this reason postischemic function was chosen for examination of the protective ability of the Euro-Collins-solution and the HTK-solution during a two-hour reperfusion period. We perfused 57 dog kidneys either with the Euro-Collins- or with the HTK-solution prior to ischemia. Ischemia was 7, 60, 90 and 120 min after Euro-Collins-perfusion and 7, 120, 150 and 180 min after HTK-protection. The protected and ischemic kidneys were left in-situ; the mean ischemic temperature was therefore 20-25 degrees C for the shorter ischemic times and 30-34 degrees C for the longer ischemic times. We compared the protected and ischemic kidneys with 14 untreated kidneys (control). Postischemic renal blood flow (RBF) was measured by an electromagnetic flow probe; renal oxygen consumption (V02/min) was calculated by arterio-venous oxygen content difference and the renal blood flow. If urine could be collected, the glomerular filtration rate (GFR) was measured by an endogenous creatinine clearance. In Euro-Collins-protected kidneys after 60-120 min ischemia the RBF was after 15 min of reperfusion between 20 and 100 ml/min/100 g. After 30 min we got values of 100-200 ml/min/100 g. The V02/min, which was in the control kidneys between 5-6 ml/min/100 g, was about 2 ml/min/100 g.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

RET receptor tyrosine kinase isoforms in kidney function and disease.

The RET proto-oncogene encodes two major isoforms, RET9 and RET51, which differ at the carboxyl-terminal. Loss-of-function mutations in RET result in gut aganglionosis while gain of function mutations result in cancer syndromes. From studies on transgenic mice, RET9 is important for early development of the kidney and the enteric nervous system. Little is known about the function of RET isoforms in later life. Here we report the expression of RET isoforms and its signalling complex, GDNF and GFRalpha1, in foetal and adult human kidneys. We found their expression in both the developing and the adult renal collecting system. We further show that only RET51 but not RET9 could promote the survival and tubulogenesis of mIMCD3 (mouse inner medullary collecting duct) cells in collagen gel. Our results agree with the hypothesis that RET51 signalling is related to differentiation events in later kidney organogenesis. In addition, it may also have a function in the adult kidney. We further extend our study by showing increased RET and GDNF expression in collecting duct cysts of polycystic kidney patients. This suggests that GDNF/RET signalling may contribute to proliferation of the collecting duct epithelium in an autocrine/paracrine manner.

Aged↗
PubMed1997

[Monitoring kidney function in patients with essential hypertension treated with enalapril].

Hypertension may to be both, cause and the results of the renal dysfunction. The N-acetyl-glucosaminidase (NAG) is a lysosomal enzyme of renal proximal tubular cells. An elevation of the enzyme activity in urine was observed in kidney diseases and also in hypertension. The aim of our study was the evaluation of the influence of the 6-months-lasting enalapril therapy on function of renal tubules and glomeruli in patients with essential hypertension. This study included 30 patients with essential hypertension (I-II grade according to WHO criteria), divided into two groups according to the initial NAG activity in urine: I-with normal NAG activity, II-with elevated NAG activity. Enalapril administered in doses 2.5-10 mg per day. The urine NAG activity, the urine and serum creatinine concentrations, the urea serum concentration and the creatinine clearance were determined after 2, 4, 8 weeks, 3 and 6 months of enalapril therapy. Simultaneously, the blood pressure and the heart rate were measured and the resting ECG was registered. In the course of the 6-months enalapril therapy of hypertension, NAG activity in urine in the group II was declined to normal values, the creatinine concentration in the urine increased in groups I and II, and the blood pressure was significantly reduced. The results of our study imply that the monitoring of the NAG activity in urine during the enalapril therapy of hypertension, may to be a indicator of protective action of the drug on the kidney and its antihypertensive efficacy.

Acetylglucosaminidase↗
PubMed1981

Renal fluoride excretion: experimental evaluation of the role of extracellular volume status during intact and impaired kidney function.

The renal disease of inorganic fluoride was studied in 5/6-nephrectomized and kidney-intact rats in order to evaluate the influence of the extracellular fluid volume status on net tubular fluoride reabsorption. Loss of renal functional mass impaired the ability of the hydropenic uremic rat to excrete fluoride, although tubular reabsorption of fluoride was depressed. Fractional fluoride excretion was closely correlated to urinary flow rate in hydropenic rats; no influence of urinary pH from 5.80 to 6.18 could be demonstrated. Acute, moderate expansion of the extracellular fluid volume by isotonic saline was followed by a significant rise in fractional fluoride excretion in uremic as well as in control rats, indicating that extracellular fluid volume is an important physiological determinant of passive tubular fluoride reabsorption.

Animals↗
PubMed2001

Effect of chronic lead exposure on kidney function in male and female rats: determination of a lead exposure biomarker.

Several cytotoxic chemical pollutants inducing peroxidative damages are liable to induce kidney failure. Among these pollutants we find heavy metals such as: lead, nickel, cadmium, vanadium and mercury. Lead is one of the most dangerous metals because it is widely spread in the environment, and because it may be a source of several nervous diseases. The aim of this study is to provide evidence concerning the effect of this metal on the renal function and to try to determine a storage corner in the organism which serves as an indicator of a lead intoxication. Lead acetate was administered by oral route in the drinking water to adult rats aged three months at the rate of 0.3% (P1) and 0.6% (P2). Reference rats received distilled water to drink under the same conditions. The treatment continued for 15, 30, 45, 60 and 90 days. The creatinemia, uremia, glycemia and creatinuria are determined by colorimetric techniques. Lead concentration in blood as well as the lead content of the tail are determined by atomic absorption after nitroperchloric mineralization at the liquid stage. The results showed an increase of creatinemia on the 30th day of the experiment for both sexes in (P1 and P2). The same happened for ureamia. The increase of these two parameters would indicate a renal deficiency which is confirmed by a decrease of creatinuria and urinary pH observed mainly on and after the 45th day of the experiment. An increase of the renal relative weight was noticed in P1 and P2 on the 30th day of the treatment. The determination of the concentration of lead in the blood shows that this factor increases among treated subjects in a constant way, independently of the dose and the duration of the treatment. Nevertheless, the rate increase of lead in the tail seems to be dose-dependent. In conclusion, lead administered by oral route causes a renal deficiency to the rat without distinction between males and females. In addition, the tail seems to be a reliable exposure biomarker that demonstrates lead intoxication. The tail seems to be a dosimeter of lead bio-accumulation. It constitutes an endogenous source of lead impregnation. The concentration of lead in the blood is only an indicator of recent exposure.

Animals↗
PubMed2000

[Terrestrial adaptation and diversity of the kidney functions in the evolution of vertebrates, Amphibia].

The Amphibia bridge the phyletic gap between the aquatic fishes and the terrestrial vertebrates. This transition has involved many interesting changes of metabolisms. In this short review, we have attempted to summarize the kidney structure and functions on the osmoregulations in the Amphibia. Amphibians excrete the water absorbed through their skin as a dilute urine. Pronephros of tadpoles may start to work in the hatching stages and metanephros is well developed and functions. Glomerular filtration rate is relatively large and glomerular intermittency is important to regulate urine production. The proximal tubule reabsorbs approximately 20-45% of filtered water and sodium. Absorption is driven by the basolateral Na+, K(+)-ATPase common to all tubular cells. The diluting segment, early parts of distal nephron, highly develops basolateral interdigitation and reabsorbs approximately 40% of filtered Na+, K+, and Cl-, but is impermeable to water, thus this part results in the formation of hypo-osmotic tubular fluid. In the late distal tubule, the primary mechanism of reabsorption may be via a luminal NaCl synporter, driven by the ubiquitous Na+, K(+)-ATPase on basolateral membrane. In collecting tubule, there are two types of cells, the principal cells and the intercalated cells. Many hormonal and nervous regulations are involved in the glomerular filtration rate and reabsorptions in the amphibian nephrons.

Adaptation, Biological↗