Hypermyoglobinemia after successful arterial embolectomy

Myoglobin concentrations in serum and urine were measured in eight patients who underwent successful arterial embolectomy in the femoral or iliac arteries. Median serum myoglobin levels significantly increased after revascularization to a maximum of 4741 micrograms/L (reference range: 0 to 80 micrograms/L) 2 hours postoperatively, with a concomitant and correlated increase in the urine myoglobin concentration. Three days after the operation, serum myoglobin concentrations were still substantially elevated in three patients. None of our patients suffered permanent renal damage, but transient renal impairment was noted in five patients, as evaluated from the serum and urine beta 2-microglobulin concentrations. We found an association between the concentrations of myoglobin in serum and urine (Spearman's rho: 0.66; p less than 0.001) and between the concentrations of myoglobin in urine and beta 2-microglobulin in urine (Spearman's rho: 0.65; p less than 0.001). Our results indicate a transient renal impairment associated with hypermyoglobinemia and myoglobinuria, even after successful arterial embolectomy.     

Urinary excretion of monocyte chemoattractant protein-1 in autosomal dominant polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD) progresses to renal insufficiency in >50% of patients and is characterized by interstitial inflammation and fibrosis in the end stage. In a rat model of ADPKD, monocytes accumulate within the renal interstitium in association with increased levels of monocyte chemoattractant protein-1 (MCP-1) in cyst mural cells and increased excretion of this chemokine into the urine. For determining the extent to which this chemokine is abnormally expressed in patients with ADPKD, a cross-section study was performed of MCP-1 in urine, serum, and cyst fluid and MCP-1 production by mural epithelial cells cultured from the cysts of human patients with ADPKD. Upper boundaries for urinary MCP-1 excretion (>263 pg/mg creatinine) and serum creatinine concentration (>1.5 mg/dl) determined in 19 normal individuals were used to sort 55 ADPKD patients into three groups. In group 1 (n = 13), urine MCP-1 excretion (136 +/- 14 pg/mg creatinine) was not different from normal volunteers (152 +/- 16 pg/mg); serum creatinine levels and urine total protein excretion were normal as well. In group 2 (n = 27), urine MCP-1 excretion was increased (525 +/- 39 pg/mg creatinine), but serum creatinine levels and urine protein excretion were not different from normal. In group 3 (n = 15), urine MCP-1 excretion increased further (1221 +/- 171 pg/mg), serum creatinine levels increased to 4.3 +/- 0.8 mg/dl, and urine protein excretion rose to 0.64 +/- 0.28 mg/mg creatinine. Serum MCP-1 levels of ADPKD patients (84 +/- 9.9 pg/ml; n = 15) did not differ from normal. Levels of MCP-1 much higher than in serum or urine were found in cyst fluids obtained from nephrectomy specimens (range, 767 to 40,860 pg/ml; mean, 6434 +/- 841 pg/ml; n = 73). Polarized, confluent cultures of ADPKD cyst epithelial cells secreted MCP-1 into the apical fluid to levels eightfold greater than in the basolateral medium. Similar results were obtained with tubule epithelial cells cultured from normal human renal cortex. On the basis of these results, it is concluded that urinary excretion of MCP-1 is increased in the majority of adult patients with ADPKD and that the source of some of this chemokine may be the mural epithelium of cysts. Furthermore, it seemed that urinary MCP-1 excretion may have increased in these ADPKD patients before appreciable increases in serum creatinine concentration or urine protein excretion were detected. It is reasonable to include urine MCP-1 excretion among candidate surrogate markers in controlled, longitudinal studies of ADPKD.     

Elevated plasma levels of the immunosuppressive complement fragment Ba in renal failure.

The complement fragment Ba is a 33 kD activation product of factor B which suppresses human B-lymphocyte functions in vitro. We report that plasma levels of Ba are highly elevated in patients with chronic renal failure (4.84 +/- 3.58 micrograms/ml) and in patients with end-stage renal disease undergoing regular hemodialysis (16.1 +/- 6.1 micrograms/ml) as compared to normals (1.01 +/- 0.30 micrograms/ml). Ba levels were strictly correlated with the creatinine clearance. The urinary excretion of Ba was 165-fold higher in patients with tubular proteinuria than in normals. These results indicate that the kidney is the major catabolic site for Ba. In addition, direct evidence was obtained for an enhanced turnover of the alternative pathway of complement in renal failure that, although it appears to be less important than the renal retention of Ba, contributes to elevated Ba plasma levels in these patients. Ba concentrations in dialysis patients who responded to hepatitis B vaccination were significantly lower than in non-responders. Furthermore, the in vitro IgM synthesis by purified mononuclear cells was negatively correlated with Ba concentrations determined in the plasma of these patients. These results suggest that the accumulation of Ba contributes to the defective immune response in patients with renal failure.     

Absence of effect of 24,25-dihydroxycholecalciferol on serum immunoreactive PTH in patients with persistent hyperparathyroidism after renal transplantation

Three hypercalcemic renal transplant recipients with stable, excellent renal function (creatinine clearance 74 +/- 11.8 ml/min) were treated with 60 micrograms 24,25(OH)2D3 by mouth daily for three months. Immunoreactive c-terminal PTH, intact PTH, 1,25(OH)2D3, 25(OH)D3, 24,25(OH)2D3, and serum and 24 h urine calcium, phosphate, magnesium and creatinine were obtained before, at one week, one month and three months of treatment, and at six weeks post-treatment. Significant elevations in serum levels of 24,25(OH)2D3 were induced by therapy (1.32 +/- .16 ng/ml to 30.06 +/- 5.18 ng/ml at one month). Moderate elevations of c-terminal PTH and normal levels of intact PTH remained unchanged throughout the study. Serum calcium remained elevated, serum phosphate and magnesium remained depressed and creatinine clearance and urinary excretion of calcium, phosphate, and magnesium remained unchanged. Furthermore, 1,25(OH)2D3 and 25(OH)D3 remained in the normal range throughout the study. We conclude that 24,25(OH)2D3 did not have a suppressant effect on levels of iPTH in the clinical setting of persistent hyperparathyroidism after successful renal transplantation.     

Elevation of serum and urine levels of TIMP-1 and tenascin in patients with renal disease.

BACKGROUND: Chronic kidney disease is characterized by increased synthesis and inhibited destruction of collagenous and non-collagenous matrix proteins. Elevation of collagen fragments has been demonstrated in the serum and urine of patients with renal disease, but the dynamics of renal matrix deposition remain difficult to determine. METHODS: To obtain a further insight into renal matrix metabolism we have assessed whether serum and urine concentrations of the non-collagenous protein, tenascin, and of the tissue inhibitor of metalloproteinases 1 (TIMP-1) are altered in association with renal disease. Serum and urine concentrations of both proteins were determined using a newly developed magnetic particle enzyme immunoassay and were compared with levels of N-terminal procollagen III-peptide (PIIINP) and related to the degree of renal failure and proteinuria. RESULTS: Circulating levels of tenascin and TIMP-1 were moderately, but significantly, higher in patients with chronic renal disease (n=54; mean creatinine clearance, 62 ml/min) than in healthy controls (n=176). Urine concentrations per mg creatinine of tenascin and TIMP-1 were significantly lower than serum levels, but were on average six- and 18-fold higher, respectively, in patients with renal disease than in controls. Urinary concentrations increased with progressive reduction in renal function, but were unrelated to proteinuria. TIMP-1 concentrations in urine correlated with tenascin, which is compatible with the impact of TIMP-1 on the accumulation of matrix proteins. The concentrations of proteins measured did not differ depending on the aetiology of renal disease. CONCLUSION: Urinary concentrations of tenascin and TIMP-1 are elevated in association with renal disease and may reflect specific aspects of renal fibrosis.     

Urinary epidermal growth factor excretion in children with chronic renal failure.

To investigate the excretion of urinary epidermal growth factor (EGF) in children with chronic renal failure (CRF), we have measured the urinary EGF/creatinine ratio (EGF/Cr) and the 24-hour urine EGF concentration in 19 children with CRF, 11 children with kidney disease and normal creatinine clearance, and 12 healthy children. Children with CRF had a significantly lower daily urine EGF concentration as well as urinary EGF/Cr. In contrast, children with kidney disease and normal renal function had normal daily urine EGF levels and urinary EGF/Cr. Accompanied by no difference in serum EGF between these two groups of patients, these data provide indirect evidence of the kidney as a source of human urinary EGF. There was a positive correlation of urinary EGF/Cr with creatinine clearance in all renal patients (r = 0.608, n = 30, p < 0.001). A much better correlation was found between daily urine EGF and creatinine clearance (r = 0.855, n = 30, p < 0.001). Our results implicate that there is a functional relationship between glomerular filtration and urinary EGF excretion, and that the urinary EGF/Cr may be a reliable indicator of urinary EGF excretion in children with CRF.     

Effect of demeclocycline on renal function and urinary prostaglandin E2 and kallikrein in hyponatremic cirrhotics

8 cirrhotics with hyponatremia were given demeclocycline (DMC) 900 mg/day to investigate its effect on renal function, plasma renin activity, aldosterone and urinary excretion of prostaglandin E2 and kallikrein. In 7 patients DMC induced an increase of free water clearance (from -0.36 +/- 0.06 to 0.13 +/- 0.06 ml/min) and serum sodium concentration (from 125.4 +/- 0.09 to 131.1 +/- 1.0 mEq/l, mmol/l). In 5 of these patients DMC also induced a marked reduction of glomerular filtration rate (from 72.2 +/- 6.2 to 31,2 +/- 4.7 ml/min) and renal plasma flow (from 468 +/- 98 to 195 +/- 55 ml/min) which could not be explained on the basis of hypovolemia. In each case this renal impairment was not associated with changes in urinary concentration of beta 2-microglobulin, urinary casts excretion, fresh urine sediment or urine protein content and disappeared after discontinuation of the drug. DMC induced a marked increase in the urinary excretion of prostaglandin E2 (from 0.82 +/- 0.27 to 6.16 +/- 1.91 ng/min) in 6 out of the 7 patients who responded to DMC and a marked reduction in urinary kallikrein (from 16.1 +/- 4.4 to 4.2 +/- 1.6 pkat/min) in the 5 patients who developed renal insufficiency. The serum DMC concentration was greater than 5 micrograms/ml in all patients who responded to DMC, greater than 8 micrograms/ml in all cases who developed renal insufficiency and of 3 micrograms/ml in the case not responding to DMC. (ABSTRACT TRUNCATED AT 250 WORDS)     

The role of thromboxane and prostacyclin in ciclosporin-induced nephrotoxicity.

The aim of the study was to determine the influence of ciclosporin (Cs) on prostacyclin and thromboxane generation. Four groups of patients were studied. Group 1: Controls, n = 10. Group 2: Patients without kidney disease treated with Cs, n = 10. Group 3: Patients after transplantation treated with azathioprine, n = 10. Group 4: Renal transplant recipients receiving Cs, n = 10. Parameters investigated: CIn, CPAH, TxB2 in plasma, serum and urine; 6-oxo-PGF1 alpha in plasma and urine, urinary 2,3-dinor-TxB2 excretion. CPAH and CIn were significantly decreased during Cs treatment. Plasma TxB2 levels were enhanced in patients without kidney disease receiving Cs (group 2) amounting to 189 +/- 106 pg/ml as compared to 12 +/- 4 pg/ml in controls (group 1). In patients without kidney disease (group 2), plasma 6-oxo-PGF1 alpha was increased (20 +/- 9 pg/ml) as compared to controls in group 1. Plasma TxB2 and plasma 6-oxo-PGF1 alpha were increased in renal graft recipients without any difference due to different immunosuppressive drugs. Treatment with Cs was associated with impaired renal function and resulted, in patients without kidney disease, in elevated plasma TxB2 and plasma 6-oxo-PGF1 alpha. This effect could not be proven in renal graft recipients. We suggest that the deleterious effect of Cs on kidney function is presumably not paralleled by corresponding changes in prostaglandin and thromboxane formation.     

Residual renal function in hemodialysis patients may protect against hyperaluminemia

We investigated 106 home hemodialysis patients whose mean [+/- SEM] serum aluminum (Al) concentration was 60.9 +/- 4.1 micrograms/liter. Serum Al concentration was inversely related to daily urine output (r = -0.52, P less than 0.001). Urine volume and measurements of Al exposure were included in a multivariate analysis of serum Al concentration in the 62 patients whose urine output was greater than 10 ml/day. The multiple correlation coefficient (r) was 0.70 (P less than 0.001) and the percentage contributions to r2 (indicating the relative importance of each factor) were: urine output 57%, oral Al intake 36%, total dialysis hours 7%. The additional contribution from cumulative water Al was negligible. In a subgroup of 26 patients with a urine output exceeding 10 ml/day, urinary Al excretion averaged 15.4 micrograms/day, and renal Al clearance and serum Al concentration were inversely related (r = -0.69, P less than 0.001). We conclude that Al-containing phosphate binders were a more important source of Al than was dialysate in these patients and that residual renal function can reduce the severity of hyperaluminemia in hemodialysis patients.     

Urinary albumin, transferrin and iron excretion in diabetic patients.

The present study was undertaken to determine urinary and serum iron, transferrin and albumin levels in diabetic patients with varying amounts of proteinuria. A highly significant correlation was found between urinary albumin and transferrin excretion over a wide range of urinary albumin excretion (0.005 to 18 g/g creatinine) (r = 0.972). The urine/serum ratio of transferrin and albumin were identical, documenting a similar glomerular leak and tubule handling for these two proteins. In contrast to the above correlation between transferrin and albumin, there was no correlation between iron and either of these proteins until nephrotic range proteinuria had occurred, and even at that time the correlation was much weaker than that found between the proteins (r = 0.680). Urinary iron excretion increased early in the course of diabetic renal disease, being increased in 3 of 11 patients without proteinuria and in 8 of 10 patients with mild proteinuria. All patients with nephrotic range proteinuria had markedly increased urinary iron excretion (150 +/- 166 micrograms/g creatinine vs. 6.4 +/- 0.7 micrograms/g creatinine in controls) and decreased serum iron levels (592 +/- 189 micrograms/liter vs. 979 +/- 394 micrograms/liter in the control group). The iron/transferrin ratio in urine was consistently greater than the iron/transferrin ratio in plasma at all stages of proteinuria. In patients with both subnephrotic and nephrotic range proteinuria, approximately 35 to 40 micrograms Fe/g creatinine was present in the urine with an excess of transferrin. In conclusion, urinary iron excretion is increased early in the course of diabetic renal disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinicopathological study on the relationship between appearance of type I or III collagen in IgA nephropathy]

This study was designed to determine whether or not the appearance of type I or type III collagen in glomeruli and serum procollagen III peptide (PIIIP) concentration are affecting the prognosis of patients with IgA nephropathy. In cases with reduced creatinine clearance (Ccr < 80 ml/min) at the time of renal biopsy, the appearance of type III collagen increased, and subsequently type I collagen appeared as Ccr decreased. In addition, we measured serum PIIIP concentration in these cases. The increase of serum PIIIP correlated with the decrease of Ccr. These results suggest that the appearance of type I and III collagen in glomeruli and the increase in serum PIIIP concentration might be a useful marker to predict the outcome of IgA nephropathy.     

Renal excretion and cyst accumulation of beta 2microglobulin in polycystic kidney disease

To determine the extent to which proximal tubule function is altered beta 2microglobulin (beta 2m), creatinine and Na were measured in serum, urine and cyst fluid of patients with autosomal dominant polycystic kidney disease and various degrees of renal insufficiency. Fractional excretion (FE beta 2m) was 0.11 +/- 0.03% in six normal subjects and 0.13 +/- 0.05% in nine patients with serum creatinine levels less than 1.6 mg/dl. In five patients with serum creatinine levels above 3.0 mg/dl, FE beta 2m was elevated (range 3.5 to 196%) and serum levels were higher than normal (30,600 +/- 6,910 micrograms/liter vs. 1,268 +/- 111). In seven patients beta 2m levels in 33 proximal cysts (cyst/serum Na greater than 0.8) equalled those in serum (cyst/serum beta 2m 0.98 +/- 0.20), whereas in 21 distal cysts (cyst/serum Na less than 0.4) beta 2m was less than in serum (cyst/serum beta 2m 0.17 +/- 0.07). Analysis of fluid in two patients with polycystic kidney nephrectomy several weeks posttransplant indicated that proximal cyst epithelium is permeable to beta 2m, but less so than to creatinine or urea. These studies show that proximal cysts cannot develop or maintain gradients for beta 2m, whereas distal cysts maintain low levels of the protein despite end-stage renal failure. The normal FE beta 2m values in nonazotemic autosomal dominant polycystic kidney disease patients and the low distal cyst levels of beta 2m in end-stage kidneys indicate that the cystic proximal nephrons do not contribute appreciably to the final urine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum Tamm-Horsfall glycoprotein level in children with various renal diseases.

Serum Tamm-Horsfall glycoprotein (THGP) concentrations were measured by a competitive enzyme-linked immunosorbent assay using peroxidase-labeled THGP in 168 patients, aged 10.5 +/- 4.6 years, with various renal diseases. Using this method, THGP was determined in the concentration range of 10-10(3) micrograms/l. Serum THGP levels ranged from 130 to 350 micrograms/l in 32 control subjects, aged 1-16 years with normal renal function. In most patients with renal disease, the serum THGP levels were lower than those in control subjects. In particular, the serum THGP levels were more reduced according to the decrease in the clearance values of endogenous creatinine (CCR). These findings suggested that the measurement of serum THGP levels is helpful in the evaluation of renal function. On the other hand, 3 patients with vesicoureteric reflux showed higher serum THGP levels than control subjects, though the CCR values in 1 of these patients was lower. These high serum THGP levels may be the result of urinary backflow into circulation.     

尿sCD146与慢性肾脏病的关系及其临床意义的探讨

目的:探讨尿sCD146水平在慢性肾脏病(CKD)中的意义及其与肾功能相关指标的关系。方法:入选105例CKD患者,CKD1期28例,CKD2期27例,CKD3期16例,CKD4期14例,CKD5期20例,(非透析患者)。设健康对照组20例。采用ELISA法检测尿sCD146水平。分析尿sCD146在CKD各期中的变化及其与肾功能相关指标的关系。结果:CKD1～5期患者尿sCD146水平均较对照组升高。各组CKD患者尿sCD146水平[CKD1(139.53±7.69)ng/ml,CKD2(156.02±15.37)ng/ml,CKD3(174.87±2.55)ng/ml,CKD4(190.66±8.01)ng/ml,CKD5(211.76±22.99)ng/ml],均显著高于对照组(128.09±4.05)ng/ml。尿sCD146水平随着CKD1～5期进展升高,P<0.05。CKD3～5期患者超敏C-反应蛋白(hs-CRP)较对照组升高、且随着CKD的进展进行性升高(P<0.05)。相关分析显示尿sCD146与血sCD146、Scr、BUN、β2-MG、CysC、hs-CRP水平呈正相关(r分别为:0.697,0.699,0.871,0.755,0.524、0.414),与eGFR、Hb、Alb呈负相关(r分别为:-0.787,-0.601,-0.298)。结论:尿sCD146与肾功能水平密切相关,可能反映早期肾功能的损伤及严重程度,并与CKD患者机体的炎症状态相关。外周血、尿液中有sCD146的异常表达,可能参与了肾脏损伤的免疫机制,能否作为检测CKD患者早期肾功能损伤新的敏感性标志物,仍需要更多样本的临床研究证实。     

Patients with autosomal dominant polycystic kidney disease have elevated fibroblast growth factor 23 levels and a renal leak of phosphate

Fibroblast growth factor 23 (FGF23) and parathyroid hormone blood levels rise following progressive loss of renal function. Here we measured parameters of phosphate metabolism in 100 patients with autosomal dominant polycystic kidney disease (ADPKD) in stage 1 or 2 of chronic kidney disease, 20 patients with non-diabetic chronic kidney disease, and 26 with type 2 diabetes. Twenty healthy volunteers served as controls. The mean levels of FGF23 were significantly (4-fold) higher in ADPKD compared to non-diabetic and diabetic patients, and healthy volunteers. Mean serum phosphate levels were significantly lower in ADPKD patients compared to non-diabetic and diabetic patients, and the healthy volunteers. The prevalence of hypophosphatemia was 38, 25, 27, and 5% in ADPKD, non-diabetic and diabetic patients, and healthy volunteers, respectively. The tubular maximum of phosphate reabsorption per glomerular filtration rate was lowest in ADPKD patients with a significantly high positive correlation with serum phosphate levels. Estimated glomerular filtration rates were approximately 100 ml/min per 1.73 m2 in all groups and parathyroid hormone and vitamin D metabolite levels were in the normal range. Thus, FGF23 was substantially elevated in ADPKD patients compared to other CKD patients matched for glomerular filtration rate, and was associated with increased renal phosphate excretion. The mechanism for this anomaly will require further study.     

Increased levels of plasma amylin in advanced renal failure.

Amylin, a 37 amino acid polypeptide, has been suggested to play a prominent role in the pathogenesis of insulin resistance in type II diabetes mellitus. Various studies have demonstrated most recently that amylin is cosecreted with insulin. No data are available on the elimination of amylin from the circulation. We therefore tested plasma levels of amylin, insulin and C-peptide in 49 non-obese, non-diabetic patients (27 male/22 female) with various degree of renal impairment (Group A: CCr less than 20 ml/min, n = 20; Group B: CCr 20-89 ml/min, n = 18; and Group C: CCr greater than 80 ml/min, n = 9). We found a significant increase of plasma amylin when kidney function, expressed by creatinine clearance fell below 20 ml/min (17.9 +/- 1.7 vs. 12.2 +/- 0.8 vs. 8.8 +/- 1.2 pg/ml; p = 0.0005). Plasma amylin correlated closely with serum C-peptide (r = .764; p = 0.0001), and to a lesser extent with insulin (r = .595; p = 0.0001) underlining its postulated cosecretion with these peptides. The data indicate that amylin might be eliminated by renal mechanisms. Our data show that besides type II diabetes mellitus, advanced renal failure is another clinical situation with enhanced plasma amylin levels. Whether amylin plays any pathogenetic role in renal patients remains to be elucidated.     

Altered IgG(4) renal clearance in patients with inflammatory bowel diseases. Evidence for a subclinical impairment of protein charge renal selectivity.

BACKGROUND:A loss of intestinal glycosaminoglycans (GAGs) has been shown in inflammatory bowel diseases (IBD). Since GAGs are involved in the regulation of renal protein filtration and GAGs disruption is associated with anionic proteinuria, we examined whether changes in the selectivity of renal protein filtration occur in IBD. METHODS:From 46 patients with IBD (17 with Crohn's disease (CD), and 29 with ulcerative colitis (UC)) and 21 healthy subjects, urine and serum samples were obtained. Albumin, total IgG and IgG(4) clearances were measured using sensitive methods. Serum p-ANCA and TNF-alpha were tested. RESULTS:Median IgG(4) clearance was 0.041 ml/ min/10(-3) in patients with UC and 0.10 ml/ min/10(-3) in CD patients, both significantly higher than in controls (0.03 ml/min/10(-3)) (P<0.03). IgG(4) clearance was above the upper normal limit in 9/17 CD (53%) and in 10/29 UC (34.5%). Eighteen of 19 patients showing abnormal IgG(4) clearance were taking mesalazine. In patients on maintenance oral mesalazine, IgG(4) clearance was higher than that in patients off treatment (0.12 vs 0.03 ml/min/10(-3), P=0.04). No clinical/laboratory sign of renal dysfunction was documented in patients with altered IgG(4) clearance and maintained on mesalazine treatment. CONCLUSION:Renal protein charge permselectivity is impaired in 40% of patients with IBD with no overt proteinuria. Our data suggest that altered IgG(4) clearance may represent a subclinical marker of renal involvement in IBD.     

Determining 'true' glomerular filtration rate in healthy adults using infusion of inulin and comparing it with values obtained using other clearance techniques or prediction equations

OBJECTIVE: To determine 'true' glomerular filtration rate (GFR) in healthy adults as renal clearance following infusion of inulin, and compare that result with those obtained using other markers and clearance techniques and with estimations of GFR using creatinine-based prediction equations. MATERIAL AND METHODS: Twenty healthy volunteers (11 females) with a median age of 27 years (range 19-36 years) received bolus doses of inulin and iohexol i.v. and 16 blood samples were taken after injection. Then, inulin and iohexol were infused to give stable plasma concentrations and blood and urine samples were collected. Residual bladder volume was estimated using ultrasound scanning. Plasma and urine concentrations of inulin and iohexol were determined using chromatography and resorcinol methods, respectively. Different methods of GFR determination were compared as well as four formulae for GFR estimation based on serum creatinine. RESULTS: 'True' GFR, i.e. renal clearance of inulin during its infusion, was a median of 117 ml/min/1.73 m2 (inter-quartile range 106-129 ml/min/1.73 m2). Similar values of GFR were obtained with renal clearance of iohexol during its infusion and also with plasma (body) clearance of inulin or iohexol following bolus injections and using 16 or five plasma samples. Endogenous creatinine clearance was higher (p<0.001) than true GFR (median 23 ml/min/1.73 m2). Plasma clearance of iohexol and inulin based on their concentrations in four blood samples underestimated their renal clearance considerably. All four creatinine-based formulae markedly underestimated renal inulin clearance. CONCLUSIONS: Plasma and renal clearance of iohexol and inulin were similar in healthy adults. Underestimation of GFR was noted when plasma clearance of iohexol and inulin was based on four but not five or more blood samples. Some prediction equations underestimate true GFR to such an extent that caution must be taken when using them to evaluate normal or high GFR values.     

Impaired renal hemodynamic but conserved natriuretic response to dopamine in patients with renal disease

Renal hemodynamics and sodium excretion were determined before and during infusion of dopamine in doses ranging from 0.25 to 8 micrograms/kg/min in healthy volunteers (n = 15) and in patients with renal disease and moderately impaired renal function (n = 21, baseline glomerular filtration rate 34-85 ml/min). While in normal volunteers dopamine resulted in marked renal vasodilation (maximal fall in filtration fraction 24%), in patients with moderately impaired renal function, the renal vasodilatory response to dopamine was impaired (maximal fall in FF 13%) and was found to depend on baseline glomerular filtration rate. Infusion of dopamine in doses of 2 micrograms/kg/min and higher resulted in an increase in urinary sodium excretion, which was comparable for healthy volunteers and patients with renal disease. We conclude that dopamine results in a predominantly efferent glomerular vasodilation and, therefore, may be salutary in lowering intraglomerular hypertension. However, in patients with renal disease the renal hemodynamic response to dopamine infusion is impaired compared to healthy volunteers, while the natriuretic response is maintained.     

Clinical study concerning of latamoxef concentration in the obstructed urinary tract

Urinary LMOX concentration was studied in 18 patients with unilateral ureteral obstruction. The concentration of LMOX in the urine from the mild obstructed kidney was 124 to 2,140 micrograms/ml and 10 micrograms/ml in the severely obstructed ones. The difference was probably due to the intensity and the duration of the obstruction. The patient with 99mTc-DMSA renal uptake of less than 3% also had a urinary LMOX concentration of less than 7 micrograms/ml. The above results seem to show that 7 micrograms/ml in urinary LMOX concentration is a significant figure for treatment of UTI. 99mTc-DMSA renal uptake and renal echogram were used to estimate the excretion rate of antibiotics into the urine.