Incipient Renal Failure Research Articles

P1278DIALYSIS IN TREATMENT OF CONGESTIVE HEART FAILURE

Abstract Background and Aims The advanced congestive heart failure (CHF), may provoke functional kidney disturbances with insufficient and resistant to conservative therapy water excretion. The treatment of the chronic renal failure (CRF) with active dialysis related to ultrafiltration (UF), may overcome the renal diuretics resistance with diuresis restoration and oedema elimination. The aim of the study was to define the indications for active, discontinued UF in setting of the CHF refractory to drugs, especially in the treatment of oedema. Method We investigated 12 patients, mean age 62,4+/-5,3 years, with incipient renal failure, but advanced congestive heart failure. Seven of them were males and 5 females. The indication for discontinued UF, was the severe expressed heart failure, reduced diuresis and initial renal insufficiency. In all investigated patients, before and after each UF procedure, the serum sodium and potassium, blood urea nitrogen (BUN), creatinin and osmolality were detected. The body weight, abdominal and crural parameters were noted before and after dialysis. Results The recovery was achieved in 10 patients with CHF, but 2 patients out of 12 have not demonstrated satisfactory response to UF. The biochemical features encountered to CHF patients suggest chronic hyponatriemia, hypokalemia and hypovolemia. Proteinuria range 1,2 to 3,6 g/l, was present in 6 patients. The clinical data were performed with oedema formation, reduced diuresis and dispnea. Mean UF rate achieved after several dialysis was 12,4+/- 7,6, lit. Conclusion Chronic heart failure in chronic renal patients, with severe oedemas is an indication for UF therapy, even if the values of BUN and creatinin are not increased. Reduction of the body weight and the extracellular volume, contribute for improved survival in these patients. However the risk of complications is high and not always with successful treatment.

Time-Dependent Alterations of Vancomycin-Induced Nephrotoxicity in Mice.

Vancomycin hydrochloride (VCM) is a glycopeptide antibiotic that is commonly used against methicillin-resistant, Gram-positive cocci despite the nephrotoxic side effects. VCM-induced nephrotoxicity has been reported in 5-28% of recipient patients. Therefore, renal failure induced by VCM has become an important clinical problem. However, the exceedingly complex mechanism of VCM-induced nephrotoxicity is not fully understood. Therefore, this study was designed to clarify time-dependent alterations of VCM-induced nephrotoxicity in mice as a step toward decreasing the risks of kidney injury associated with VCM therapy. VCM was injected intraperitoneally into mice at a dose of 400 mg/kg body weight at 24-h intervals for 3, 5, 7, and 14 d. At 24 h after the last injection, we examined histopathological alterations of the kidney as well as blood biochemistry. VCM administration resulted in a decrease of body weight and increase of kidney weight. Histological examination revealed renal damage such as dilated proximal tubules with occasional casts and interstitial fibrosis in VCM-treated mice. Furthermore, immunohistochemical staining with anti-CD10 and anti-single-stranded DNA antibodies highlighted damaged renal proximal tubules with marked dilatation as well as numerous apoptotic cells as early as day 4 of VCM-treatment. The severity of symptoms progressed until day 15. These results suggest that VCM-induced renal damage and incipient renal failure begin soon after the start of treatment and progressively worsen. This is the first report describing the time-dependence of VCM-induced nephrotoxicity in mice and depicting a model that clarifies the mechanisms of this tissue damage.

Real-time monitoring of progression towards renal failure in primary care patients.

Chronic renal failure is a progressive condition that, typically, is asymptomatic for many years. Early detection of incipient kidney failure enables ameliorative treatment that can slow the rate of progression to end-stage renal failure, at which point expensive and invasive renal replacement therapy (dialysis or transplantation) is required. We use routinely collected clinical data from a large sample of primary care patients to develop a system for real-time monitoring of the progression of undiagnosed incipient renal failure. Progression is characterized as the rate of change in a person's kidney function as measured by the estimated glomerular filtration rate, an adjusted version of serum creatinine level in a blood sample. Clinical guidelines in the UK suggest that a person who is losing kidney function at a relative rate of at least 5% per year should be referred to specialist secondary care. We model the time-course of a person's underlying kidney function through a combination of explanatory variables, a random intercept and a continuous-time, non-stationary stochastic process. We then use the model to calculate for each person the predictive probability that they meet the clinical guideline for referral to secondary care. We suggest that probabilistic predictive inference linked to clinical criteria can be a useful component of a real-time surveillance system to guide, but not dictate, clinical decision-making.

Hereditary hypophosphatemic rickets with hypercalciuria: case report.

We report a case of a male aged 50 years who consulted for renal disease recurrent lithiasis and nephrocalcinosis. The clinical examination showed external signs of rickets/osteomalacia and biochemical data as well as a severe loss of renal phosphate with hypophosphatemia, normal 25 OH vitamin D, high 1,25 OH vitamin D and hypercalciuria. Parathyroid hormone was low and renal ultrasound confirmed the existence of severe bilateral medullary nephrocalcinosis. They also found incipient chronic renal failure and incomplete renal tubular acidosis, both secondary to nephrocalcinosis and unrelated to the underlying disease. The molecular study found a change in homozygosity in intron 5 of gene SLC34A3 (NM_080877.2:c[ 448 +5G>A] + [ 448 +5G>A] ). His three children were carriers of the same variant in heterozygosis and although they were clinically asymptomatic two of them had hypercalciuria. All these data suggest that the patient had hereditary hypophosphataemic rickets with hypercalciuria (HHRH) secondary to an alteration in the sodium dependent phosphate cotransporter located in proximal tubule (NaPi-IIc). The HHRH is transmitted by autosomal recessive inheritance and is an extremely rare form of hypophosphatemic rickets. The diagnosis and treatment are essential to prevent bone sequelae of rickets and nephrocalcinosis. A correct differential diagnosis with other forms of hypophosphatemic rickets has implications on the treatment, as the management based only on phosphorus supplementation usually corrects all clinical and biochemical abnormalities, except for the loss of phosphorus in the urine. The exogenous supply of calcitriol, as advised in other hypophosphatemic rickets, may induce renal calcium deposits and nephrocalcinosis and worsens the prognosis.

Intermediate Volume on Computed Tomography Imaging Defines a Fibrotic Compartment that Predicts Glomerular Filtration Rate Decline in Autosomal Dominant Polycystic Kidney Disease Patients

Total kidney and cyst volumes have been used to quantify disease progression in autosomal dominant polycystic kidney disease (ADPKD), but a causal relationship with progression to renal failure has not been demonstrated. Advanced image processing recently allowed to quantify extracystic tissue, and to identify an additional tissue component named "intermediate," appearing hypoenhanced on contrast-enhanced computed tomography (CT). The aim of this study is to provide a histological characterization of intermediate volume, investigate its relation with renal function, and provide preliminary evidence of its role in long-term prediction of functional loss. Three ADPKD patients underwent contrast-enhanced CT scans before nephrectomy. Histological samples of intermediate volume were drawn from the excised kidneys, and stained with hematoxylin and eosin and with saturated picrosirius solution for histological analysis. Intermediate volume showed major structural changes, characterized by tubular dilation and atrophy, microcysts, inflammatory cell infiltrate, vascular sclerosis, and extended peritubular interstitial fibrosis. A significant correlation (r = -0.69, P < 0.001) between relative intermediate volume and baseline renal function was found in 21 ADPKD patients. Long-term prediction of renal functional loss was investigated in an independent cohort of 13 ADPKD patients, followed for 3 to 8 years. Intermediate volume, but not total kidney or cyst volume, significantly correlated with glomerular filtration rate decline (r = -0.79, P < 0.005). These findings suggest that intermediate volume may represent a suitable surrogate marker of ADPKD progression and a novel therapeutic target.

Coronary syndrome Y: Should we focus more on extra-cardiac conditions including renal disease and its management?

⁎ Corresponding author. E-mail address: kyalta@gmail.com (K. Yalta). In their recently published article, Muxel S et al. reported amalewith coronary slow flow (CSF) as measured with increased thrombolysis in myocardial infarction (TIMI) frame counts (TFC), and comment on the different clinical presentations and pathophysiological mechanisms of coronary syndromeXandY [1].We agreewith the authors that coronary syndrome X is generally characterized by impaired coronary vasodilation andcoronaryflow reservewhile coronary syndromeYoccurs due to enhanced coronary resistance leading to CSF [1]. Endothelial dysfunction plays the central role in the pathogenesis of coronary syndrome X and Y [1] indicating their potential co-existence in a portion of cases. However, compared to isolated coronary syndrome X, coronary syndrome Y is more likely to accompany and/or be associated with extra-cardiac pathologies potentially associated with endothelial dysfunction and subclinical myocardial fibrosis, etc. The association between renal disease and coronary syndrome Y, as described below, may potentially harbour some diagnostic, therapeutic and prognostic implications, and has recently drawn particular attention in the clinical setting. Chronic renal failure (CRF) is well known to induce endothelial dysfunction and consequent coronary atherosclerosis possibly due to a variety of CRF-induced pathologies including increased levels of asymmetric-dimethylarginine (ADMA) [2], inflammatory response and oxidative stress, accompanying hypertension, etc. Similarly, coronary syndrome Y (characterized by CSF) may be encountered in the setting of CRF, and may be regarded as a marker of coronary microvascular dysfunction that is largely attributable to increased microvascular resistance associated with endothelial dysfunction, subclinical myocardial fibrosis and hypertrophy [2,3], etc. Endothelial dysfunction is alsowell known to contribute to the pathogenesis of CRF. Therefore, coronary syndrome Y, coronary atherosclerosis and CRFmay share the same clinicopathological background, to some extent indicating the complex relationship among these entities. A recently published study demonstrated significant reductions in coronary blood flow in patients with end-stage renal disease (ESRD) regardless of the degree of epicardial coronary artery stenosis [3]. In another previous study by our group including patients with mild to moderate renal dysfunction and angiographically normal coronary arteries, we were able to demonstrate significant reductions in coronary blood flow as measured with increased TFC values compared to the control group with normal coronary arteries and renal functions [2]. It is also of note that in the patient group of our study, the values of TFC and calculated glomerular filtration rate (GFR) were also found to be independently correlated [2] indicating the close link between coronary syndrome Y and renal failure. Therefore, in the clinical setting, renal failure may accompany (as a result of generalized endothelial dysfunction) and/or beassociatedwith coronary syndromeY. Even though the renal statusof the case reported by Muxel S et al. [1] was not reported, the patient might have suffered some kind of subclinical or incipient renal failure (even with normal blood-urea-nitrogen (BUN) and creatinine levels), and hence may need to be thoroughly evaluated via other diagnostic modalities (GFR calculation, renal imaging, etc.) along with subsequent close follow-up for the possible emergence or progression of renal failure. Itmay be suggested that among coronarymicrovascular syndromes, coronary syndrome Y is more likely to accompany and/or be associated with extra-cardiac conditions (renal disease, etc. even in the subclinical stage) indicating the need for thorough evaluation of patients with this syndrome via various diagnostic modalities. In the setting of coronary syndrome Y (isolated or in combination with coronary syndrome X), besides targeting enhancement of coronary bloodflow, earlier diagnosis andmanagementof associated conditions including renal failuremaybe of utmost clinical value in the management of coronary microvascular dysfunction, and may possibly improve clinical outcomes including renal and cardiac adverse events. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [4].

Iatrogenic Tracheal Laceration Causing Asphyxia

Endotracheal intubation is a simple, rapid, and safe technique that is being used as a standard procedure for airway management. However, airway injury during endotracheal intubation could be a significant source of morbidity or even mortality for patients and a source of liability for physicians as well. We report an unusual case of fatal tracheal occlusion by intraluminal blood clot complicating endotracheal intubation. The patient, a 62-year-old woman, with renovascular hypertension and incipient renal failure was scheduled for renal autotransplantation. The surgery was uneventful but the postoperative course was complicated with a lethal airway obstruction. At autopsy a linear longitudinal tracheal laceration was identified with an intraluminal blood clot obstructing the tracheal lumen. Tracheal laceration as a cause of death is a rare and potentially fatal complication of endotracheal intubation with intratracheal bleeding, clot formation, tracheal occlusion, and subsequent asphyxia.

Effect of Corticosteroid Therapy on Low-Molecular–Weight Protein Markers of Kidney Function

Serum cystatin C, β2-microglobulin, and β-trace protein are endogenous markers of glomerular filtration rate (GFR). Cystatin C, in particular, is a promising alternative to creatinine for the detection of incipient renal failure. However, corticosteroids affect the extrarenal metabolism of cystatin C, which limits the use of cystatin C as a marker of GFR in a variety of clinical settings. Low-molecular–weight (LMW) β-trace protein might be a useful alternative in this respect. The present study set out to compare the effect of corticosteroid therapy on the serum concentrations of cystatin C, β2-microglobulin, and β-trace protein. We studied a group of 108 children being treated or followed for malignancy (n = 41) or renal disease (n = 67). In the former group 14 patients (34%) were treated with glucocorticoids, in the latter 18 (27%). We compared single-injection inulin clearance studies in 76 patients not receiving steroids with 32 in patients receiving corticosteroid treatment (median dose 33.0 mg prednisone-equivalent per m2 body surface area per day, range 1.2–70.4). Mean (SD) age was 9.7 (5.8) years, mean (SD) GFR 92.8 (34.6) mL · min−1 · (1.73 m2)−1. Patients included in the …

Primary non-hodgkin lymphoma of urinary bladder with nine years later renal involvement and absence of systemic lymphoma: A case report

Primary bladder non-Hodgkin lymphoma (PBNHL) is very rare, especially as extranodal B-small lymphocytic lymphoma (B-SLL). Also, late isolated renal manifestation of PBNHL is extremely unusual. We report a very rare type of extranodal B-SLL of bladder wall with extremely unusual late isolated renal involvement, clinically manifested by nephrotic syndrome and incipient renal failure. A 56-year-old woman was presented with a solitary tumor of bladder wall, with history of dysuria and night sweating. A transvaginal needle biopsy of the tumor was performed, and diagnosis of primary extranodal B-SLL was made in the absence of bone marrow, lymph node, or blood involvement. She was treated with chemotherapy until the achievement of complete remission. Nine years later, she developed nephrotic syndrome. The renal biopsy revealed parenchymal lymphoma's involvement associated with glomerular lesion. Immunohistochemical analysis confirmed the same imunophenotype of lymphoma cells like in bladder wall nine years ago. Restaging procedure showed no evidence of disease elsewhere. To our knowledge, it is the first case of association of very rare primary bladder B-SLL with late isolated renal involvement.

Toxidermie avec manifestations systémiques et sérologie lupique induites par l’infliximab

Infliximab is a monoclonal anti-Tumor Necrosis Factor alpha-antibody (anti-TNFalpha) that has demonstrated its efficacy in the treatment of rheumatoid arthritis, Crohn's disease and psoriasis.We report the case of a 59 year-old woman with a 20-year history of rheumatoid arthritis consulting for an atypical erythematosus rash 18 months after her first infusion of infliximab. The rash was associated with inflammatory syndrome, incipient renal failure and high levels of antinuclear antibodies with the presence of anti-dsDNA antibodies. Lack of specificity in both skin manifestations and histology ruled out a diagnosis of drug-induced lupus. Discontinuation of treatment with infliximab resulted in improvement of all clinical signs together with a significant decrease of antinuclear antibody titers within six months.Induction of antinuclear antibodies and/or anti-dsDNA antibodies is often seen in patients treated with TNFalpha inhibitors. Cases of true systemic lupus erythematosus or anti-TNFalpha-related eruption in a context of autoimmunity, as seen in our patient, have been reported only rarely. All cases were reversible upon discontinuation of treatment.

A modified sigma‐rectum pouch (Mainz pouch II) technique: analysis of outcomes and complications on 220 patients

To evaluate the safety and efficacy of a modified technique for a sigma-rectum pouch (Mainz pouch II). Between October 1994 and March 2003, a modified Mainz pouch II was constructed in 220 patients (153 men and 67 women, mean age 56.7 years) in a multicentre prospective study. The median follow-up (177 patients, 81%) was 21 (1-84) months. There were no peri-operative deaths; there were early complications in 24 patients, including prolonged ileus in six, pyelonephritis in 17, unilateral ureterohydronephrosis in 11, bilateral ureterohydronephrosis in two, and incipient renal failure in five. Late complications included ureteric implantation-site stenosis (unilateral in eight patients and bilateral in three). In all, 92 patients (52%) needed oral alkalizing medications and potassium supplementation because of hyperchloraemic metabolic acidosis. All but three patients (99%) were continent by day and at night. The mean (sd) voiding frequency was 4.2 (1.6) voids by day and 2.1 (0.5) at night. The Mainz pouch II is a simple and reproducible surgical technique, with good results in terms of mortality, morbidity, continence and overall quality of life. The main limitation is malignant transformation of the uretero-intestinal anastomosis. For selected cases, the technique is a good alternative to other types of continent urinary diversion.

Use of gastric segment in urinary bladder replacement after total cystectomy

Drainage of urine by abnormal way is urinary derivation. Various forms of urinary derivations are available for urinary bladder replacement after radical cystectomy for invasive bladder tumor. Construction of continent urinary reservoir, so called pouch, from different bowel segments is named continent urinary derivations. If such urinary reservoir is connected with urethra, then it is about orthotopic derivation and reservoir is defined as neobladder. Upon satisfactory results of introduction of continent urinary derivations with Mainz pouch I and Orthotopic Mainz pouch, we performed continent orthotopic urine derivation with isolated gastric segment in 74-year old male patient who had previously undergone radical cystoprostatectomy because of the invasive urothelial cancer of the urinary bladder. Even though there were no major surgical complications in the near postoperative course, the patient had to be operated ten months later for ileus; 20 months after the procedure, significant loss of neobladder capacity, bilateral vesicoureteral reflux, persistent urinary infection and incipient renal failure were manifested. In the further course, reoperation was needed and neobladder augmentation by ileal pouch along with both ureteral reimplantations into the pouch wall was carried out. After this reintervention, the patient was alive in the following three years with satisfactory quality of life and preserved renal function. Our conclusion is that gastric neobladder should not be the first method of choice for urinary bladder replacement after radical cystectomy in older patients.

Progression of Kidney Damage in Balkan Endemic Nephropathy: A 15-Year Follow-Up of Patients with Kidney Biopsy Examination

Progression of kidney damage was studied in 18 patients with Balkan endemic nephropathy (BEN), with a mean 15-year follow-up after renal biopsy. According to kidney function, estimated by 99mTc-DTPA clearance, patients were divided into three groups: with apparently normal kidney function (clearance 103.5 ± 21.3 mL/min/1.73 m2), with incipient renal failure (clearance 65.5 ± 11.3), and with advanced renal failure (clearance 28.0 ± 6.2). The mean yearly decrease of glomerular filtration rate was 2.74 mL/min. In two patients, an increase of kidney function was recorded. Six patients become dialysis dependent, two from the group with incipient renal failure, but all four from the group with advanced renal failure. Three patients died after 8 to 12 years of follow-up, one from causes unrelated to kidney disease and two from end-stage renal failure. This study has shown that BEN is characterized by a slow course and prolonged evolution, modified by medical supervision and treatment.

Secondary hyperparathyroidism and vitamin D receptor binding to vitamin D response elements in rats with incipient renal failure.

The pathogenesis of secondary hyperparathyroidism in early renal failure is poorly understood. In the study presented here, parathyroid hormone and GFR in rats with mild renal failure of various durations are evaluated. Parathyroid hormone increased significantly 3 days after nephrectomy and peaked at 2 wk, despite reduction in GFR of < 50%. Parathyroid hormone remained elevated, but there was no difference in serum levels of calcium, phosphorus, and calcitriol between the nephrectomized and sham-operated rats. There were also no differences in both intestinal and kidney vitamin D receptor concentrations between the two groups. Histomorphometric analysis of bone at 6 wk revealed significant increase in osteoid thickness, osteoblast number, erosion surface with osteoclasts, and erosion depth. Employing electrophoretic mobility shift assay, we consistently observed a significant reduction in kidney calcitriol-receptor complex binding to mouse osteopontin vitamin D response element (-70.2 +/- 4.9%, P < 0.001). Western blot analysis also revealed a significant reduction in at least one retinoid X receptor isoform. In conclusion, biochemical and histological evidence of secondary hyperparathyroidism develops in rats with mild renal failure, despite normal calcium, phosphorus, calcitriol, and vitamin D receptor concentrations. These rats also have evidence of reduced renal vitamin D receptor binding to nuclear response elements. This finding, possibly an important early factor in the pathogenesis of secondary hyperparathyroidism, could also play a role in the development of compensatory renal growth of the remnant kidney.

Attenuated Rise of 1,25 (OH)&lt;sub&gt;2&lt;/sub&gt; Vitamin D&lt;sub&gt;3&lt;/sub&gt; in Response to Parathyroid Hormone in Patients with Incipient Renal Failure

Despite elevated parathyroid hormone (PTH) levels, low normal or diminished serum 1,25(OH)2D3 concentrations are found in patients with incipient renal failure. To further assess (indirectly) the reserve capacity of renal production of 1,25(OH)2D3 we studied 9 patients with incipient or moderate renal failure (inulin clearance 31-68ml/min/1.73 m2) and 9 controls, using a novel stimulation test. We measured 1,25 (OH)2D3 levels, free 1,25(OH)2D3 index, cAMP excretion, calciuria and phosphaturia before and after infusion of 2 x 400 U of human (h) PTH (1-38). Baseline 1,25(OH)2D3 levels were not significantly different in patients (42.5 pg/ml, 21.6-51.1) compared with controls (45.0 pg/ml, 37.4-67.3). After infusion of hPTH(1-38), however, median increase in 1,25(OH)2D3 was only +25% versus +86% in controls, despite a greater proportional increase in cAMP/GF ratio. The data suggest subnormal stimulation of renal 1,25(OH)2D3 production in response to exogenous PTH in most patients with incipient renal failure. This may reflect partial exhaustion of biosynthetic reserve capacity.

Calcium Metabolism in Early Chronic Renal Failure: Implications for the Pathogenesis of Hyperparathyroidism

Studies in the past showed elevated immunoreactive parathyroid hormone (PTH) serum values in early renal failure, but the assays used in these studies could not discriminate between bioinactive fragments of the PTH peptide and biologically active hormone. The availability of a sensitive PTH assay, which quantitates intact hormone, now allows the analysis of biologically active PTH in renal failure. To characterise more precisely the point of onset of hyperparathyroidism in the course of chronic renal failure and its relation to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], we measured plasma intact PTH and vitamin D metabolite serum values in 63 non-nephrotic uraemic patients (male n = 35, female n = 28, age 31-78 years) with incipient (GFR 60-90 ml/min per 1.73 m3, n = 19) mild (GFR 40-60, n = 22) and moderate (GFR 20-40, n = 22) renal failure, and in 22 age-matched healthy control subjects. Intact PTH concentrations were negatively correlated with GFR (r = -0.57, P less than 0.001). Median plasma intact PTH values (normal range 1.2-6 pmol/l) were 5.6 (range 2.2-13.0) in incipient, 8.1 (2.9-24.0) in mild, and 13.0 (5.4-59.0) in moderate renal failure. Intact PTH values in incipient renal failure were significantly greater than in 22 age-matched control subjects (P less than 0.01). The decline of GFR was paralleled by a progressive decrease in 1,25(OH)2D3 serum values (r = 0.44, P = 0.001). Median values of the hormone (normal range 35-90 pg/ml) were 32 (range 20-66) in incipient (P less than 0.01 vs. age-matched control subjects), 34 (22-74) in mild, and 26 (17-39) in moderate renal failure. In all three groups, mean serum phosphate and total calcium concentrations (corrected for serum protein) were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Captopril in patients with type II diabetes and renal insufficiency: Systemic and renal hemodynamic alterations

Purpose: To our knowledge, clinical studies on the long-term use of angiotensin converting enzyme inhibitors in patients with type II diabetes mellitus and nephropathy with incipient renal failure are nonexistent. We therefore assessed the effects of long-term treatment with captopril on systemic and renal hemodynamics and urinary protein excretion in patients with type II diabetes mellitus and the clinical syndrome of diabetic nephropathy. Patients and methods: Twelve patients, 10 men and two women, with an average age of 52 years (range, 40 to 66), participated in the study. After the basal hemodynamic evaluation, the patients received captopril in two daily doses. The dosage was adjusted at weekly intervals in order to obtain normalization of blood pressure without exceeding the maximum allowable dosage. Four patients also received furosemide (20 to 40 mg/day). Results: After six months of treatment, the intra-arterial blood pressure fell (from 162 ± 17 103 ± 5 to 139 ± 26 89 ± 10 mm Hg) due to the reduction in total peripheral vascular resistance index (from 3,720 ± 658 to 3,190 ± 762 dynes/second/cm −5/m 2), with no change in cardiac index (2.78 ± 0.36 to 2.79 ± 0.47 liters/minute/m 2). No significant change was seen in renal vascular resistance (from 30,175 ± 5,371 to 30,173 ± 5,372 dynes/second/cm −5/1.73 m 2) and in filtration fraction (from 26 ± 8 to 27 ± 10 percent). A slight, not significant, decrease in renal plasma flow (from 243 ± 97 to 217 ± 108 ml/minute/1.73 m 2), in glomerular filtration rate (from 57 ± 17 to 51 ± 19 ml/minute/1.73 m 2), and in proteinuria (from 4.50 ± 3.10 to 3.40 ± 2.31 g/day) was also observed. Conclusion: Our findings suggest that captopril is an effective antihypertensive agent in patients with diabetic nephropathy, but the renal beneficial effects seem to be limited when this syndrome is complicated by renal insufficiency.

The prevention of renal impairment in patients undergoing orthotopic liver grafting by infusion of low dose dopamine.

Administration of low dose dopamine (2.0 micrograms/kg/minute) begun before surgery in patients undergoing liver transplantation decreases the incidence of postoperative renal impairment. Thirty-four consecutive patients in the Cambridge/King's College Hospital liver transplantation series were studied. Nineteen patients (21 transplant operations) received prophylactic low dose dopamine throughout the operative and early postoperative period, while 15 patients (15 transplant operations) received dopamine only when clinically indicated for incipient renal failure or as an inotropic agent. In the prophylactic dopamine group, only two transplant operations (9.5%) were complicated by renal impairment, whereas in the other group, 10 patients (67%) developed renal impairment (p = 0.001); of these, four developed acute renal failure (27%). Comparison of seven pairs of patients, matched for age, sex, diagnosis, operative blood loss and operative hypotension (one group receiving dopamine, the other not), revealed a significantly higher urine output in the first 24 hours and creatinine clearance 24-48 hours after surgery (p less than 0.05) in those treated prophylactically. In view of these findings, we would recommend that consideration be given to the prophylactic use of dopamine in patients undergoing orthotopic liver transplantation.

Planning and Protecting Vascular Access Sites in the Future Hemodialysis Patient

The patient with incipient renal failure has usually undergone repeated phlebotomy, intravenous catheter insertion, or invasive monitoring through veins and arteries of the upper extremity. When finally evaluated for hemodialysis angioaccess, the patient may be found to have numerous sclerotic or thrombosed veins, inflamed catheter entry sites, resolving hematomas, or radial artery occlusion. These complications are common. In 50% of the patients referred to me for access, their anatomy has become unsatisfactory for construction of long-term dialysis access. Therefore, at the earliest sign of renal failure, the primary-care physician must consider the special problems of future hemoaccess. Precautions should be taken to keep monitoring and phlebotomy procedures away from the primary-access vessels, generally the radial artery and cephalic veins. Although short-term access may be provided through external shunts (Scribner type) from the radial artery to a forearm vein, the preferred access is the subcutaneous Brescia-Cimino radiocephalic arteriovenous fistula. This high-flow

Multicystic transformation of kidneys in chronic renal failure.

With real-time sonography, 120 nondialyzed uremic patients prior to hemodialysis, 108 patients on maintenance hemodialysis and 9 patients postdialysis after successful homotransplantation were examined for the presence of renal cysts. Even in incipient renal failure, multiple cysts were demonstrable in some patients (at a serum creatinine of 3 mg/dl in 22% of patients), particularly in patients with analgesic nephropathy. When hemodialysis was started (serum creatinine approximately 10 mg/dl), 35% of the patients had multiple cysts. On hemodialysis, the prevalence, number and size of cysts rose progressively with time. After 8 years of hemodialysis, 92% of the patients had multiple cysts. However, enlargement of the kidneys was observed in only 2/108 patients. No major clinical complications were noted with the possible exception of 1 case of renal cell carcinoma. No correlation was noted between hematocrit and presence or extent of cystic transformation, but the 2 patients with cystic enlargement of the kidneys were polyglobulic. In 8/9 patients after transplantation, cysts were demonstrable in the patient's own kidneys after a median follow-up of 16 months. On light microscopy, cysts were lined by cuboidal or columnar epithelial cells with frequent papillary or adenomatous proliferations. The cyst lumen was filled with amorphous or lamellated organic material, which exhibited microfibrillar structure on electron microscopy. One kidney examined after ex vivo perfusion fixation showed multiple interconnected cavities on scanning electron microscopy. Ultrastructural studies showed epithelia with either the characteristics of proximal tubular cells (i.e. numerous microvilli, interdigitations and abundant lysosomes or mitochondria) or distal tubular cells (i.e. highly interdigitating processes) or finally collecting duct cells (i.e. no interdigitations and few microvilli).