Course Of Chronic Renal Failure Research Articles

IPET-CT in inflammatory diseases of kidneys and bladder: diagnostic efficacy

Introduction. The incorporation of combined positron emission tomography-computed tomography (PET-CT) into clinical practice has significantly expanded the understanding of the pathogenesis of many diseases. Evidence-based data on the diagnostic efficacy in infectious and inflammatory diseases is increasing, making this imaging method very promising. Purpose of the study. To study the diagnostic efficacy of 18F-FDG PET-CT in various chronic inflammatory diseases of kidneys and bladder.Materials and methods. A retrospective study of the results of whole-body 18F-FDG PET-CT in 45 patients was carried out. Patients underwent an investigation at various times after surgical treatment of localized oncology of the anogenital zone at the T1N0M0 stage without the involvement of the genitourinary system. It was found that 24 patients had a history of chronic pyelonephritis and 21 patients had manifestations of radiation cystitis. Repeated PET/CT scans were performed after a course of therapy for inflammatory urological diseases to assess the treatment results of the underlying pathology.Results. The latent course of chronic renal failure was accompanied by a diffuse decrease in 18F-FDG metabolism in the renal parenchyma with its partial recovery after etiotropic therapy and urine sanitation. Hypermetabolism of 18F-FDG was detected in the bladder wall during manifestations of radiation cystitis, which was leveled during therapy and relief of urinary syndrome manifestations. Bacterial and radiation inflammation differed in molecular-cell responses to the pathogen, while the results of urinalysis, indicating the effectiveness of the treatment, coincided with the visual and digital indicators of the restoration of adequate energy metabolism in the studied tissues.Conclusions. Metabolism of 18F-FDG in the kidneys and bladder can objectively reflect the nature of inflammation and complement the data on the effectiveness of the treatment.

Peculiarities of the Clinical Course of Chronic Viral Hepatitis C in the Background of End-Stage Chronic Renal Insufficiency

We investigated the clinical, epidemiologic, and pathogenetic features of viral hepatitis C in hemodialysis departments. This multicenter study included patients who were seen at the hemodialysis department in Tashkent, Uzbekistan and at regional departments located in the Republic of Uzbekistan. We examined 395 patients who were on hemodialysis from 3 to 15 years. A diagnosis of chronic viral hepatitis C was made on the basis of anamnesis, clinical laboratory data, and detection of immunoglobulin G antibodies for hepatitis C virus. From clinical and laboratory results analyzed in 395 patients, markers of infection with parenteral viral infections were shown in 181 patients (45.8%). Chronic viral hepatitis C had the highest incidence among infections, which was detected in 125 patients (31.6%). With regard to chronic renal failure, 11 patients (34%) with chronic viral hepatitis C had a transient form of chronic renal hepatic failure with development of adverse outcomes. Of patients with chronic viral hepatis C infection, 13 patients (40%) with hemorrhagic syndrome developed progressive anemia and 8 patients (25%) developed persistent polyserositis in the form of hydrothorax, ascites, and pericarditis. These developments reflect the aggravating effects of chronic viral hepatitis C on the course of chronic renal failure. In our study that included patients seen at hemodialysis departments in Uzbekistan, chronic viral hepatitis C was greatly prevalent, although occurring mainly in a minimal form of the pathologic process. Chronic viral hepatitis C has an aggravating effect on the course of underlying diseases with development of adverse outcomes.

Kynurenine Pathway in Chronic Kidney Disease: What's Old, What's New, and What's Next?

Impaired kidney function and increased inflammatory process occurring in the course of Chronic Kidney Disease (CKD) contribute to the development of complex amino-acid alterations. The essential amino-acid tryptophan (TRP) undergoes extensive metabolism along several pathways, resulting in the production of many biologically active compounds. The results of many studies have shown that its metabolism via the kynurenine pathway is potently increased in the course of CKD. Metabolites of this pathway exhibit differential, sometimes opposite, roles in several biological processes. Their accumulation in the course of CKD may induce oxidative cell damage which stimulates inflammatory processes. They can also modulate the activity of numerous cellular signaling pathways through activation of the aryl hydrocarbon receptor, leading to the disruption of homeostasis of various organs. As a result, they can contribute to the development of the systemic disorders accompanying the course of chronic renal failure. This review gathers and systematizes reports concerning the knowledge connecting the kynurenine pathway metabolites to systemic disorders accompanying the development of CKD.

Secondary and Tertiary Hyperparathyroidism in Chronic Kidney Disease: An Endocrine and Renal Perspective.

Secondary Hyperparathyroidism (SHP) seen as a frequent complication in Chronic Kidney Disease (CKD) has many pathogenetic peculiarities that are still incompletely defined and understood. During the long course of chronic renal failure, SHP can also transform sometimes into the hypercalcemic state characterized by quasi-autonomous production of Parathyroid Hormone from the parathyroid glands: a disorder that is termed Tertiary Hyperparathyroidism. The clinical consequences of SHP in CKD are protean, encompassing bone and mineral abnormalities but as recently identified, also several metabolic and cardiovascular problems, the most important of which is vascular calcification. There have been several advances in the therapeutic armamentarium available for the treatment of SHP, though clear demonstration of a benefit regarding major clinical outcomes with any of the new agents is still lacking. This narrative review summarizes the current understanding about this disorder and highlights some of the recent research on the subject.

Influence of Parathyroidectomy on Bone Calcium Concentration: Evaluation with Spectral CT in Patients with Secondary Hyperparathyroidism Undergoing Hemodialysis-A Prospective Feasibility Study.

Purpose To use spectral computed tomography (CT) to evaluate the influence of parathyroidectomy (PTX) on calcium concentration in trabecular bone and cortical bone in patients undergoing hemodialysis with secondary hyperparathyroidism. Materials and Methods This study was performed with institutional review board approval. Written consent was obtained from each patient. Thirty-eight men (mean age ± standard deviation, 55.69 years ± 8.05; range, 42-72 years) undergoing maintenance hemodialysis who underwent PTX and 40 patients (mean age, 56.71 years ± 9.53; range, 45-74 years) who did not undergo PTX received prospective follow-up for 2 years. Bone calcium concentration was measured in the cortical compartment of the bilateral proximal femur and the medullary compartment of the lumbar vertebral bodies (L1 through L3) on the basis of calcium-based material decomposition images of a spectral CT examination. The differences between baseline and end-of-study PTX parameters were analyzed with the paired Student t test. Results For patients who underwent PTX, mean cortical bone calcium concentration increased from 220.69 mg/cm3 ± 25.79 to 257.43 mg/cm3 ± 25.46 (t = 8.546, P < .001), whereas medullary bone calcium concentration decreased from 64.75 mg/cm3 ± 15.07 to 61.42 mg/cm3 ± 15.77 (t = 22.293, P < .001) from baseline to follow-up. In patients who did not undergo PTX, mean cortical bone calcium concentration decreased from 296.08 mg/cm3 ± 36.35 to 258.35 mg/cm3 ± 31.46 (t = 7.420, P < .001), but medullary bone calcium concentration increased from 61.13 mg/cm3 ± 13.85 to 62.94 mg/cm3 ± 14.80 (t = 2.370, P = .023) from baseline to follow-up. Conclusion During the course of chronic renal failure, different bone elements involve various pathologic changes. PTX could reverse long-term cortical bone loss reflected in calcium concentration measured with spectral CT; however, it could induce medullary bone loss. © RSNA, 2017 Online supplemental material is available for this article.

A comparison of the long-term effects of lanthanum carbonate and calcium carbonate on the course of chronic renal failure in rats with adriamycin-induced nephropathy.

Lanthanum carbonate (LA) is an effective phosphate binder. Previous study showed the phosphate-binding potency of LA was twice that of calcium carbonate (CA). No study in which LA and CA were given at an equivalent phosphate-binding potency to rats or humans with chronic renal failure for a long period has been reported to date. The objective of this study was to compare the phosphate level in serum and urine and suppression of renal deterioration during long-term LA and CA treatment when they were given at an equivalent phosphate-binding potency in rats with adriamycin (ADR)-induced nephropathy. Rats were divided into three groups: an untreated group (ADR group), a CA-treated (ADR-CA) group and a LA-treated (ADR-LA) group. The daily oral dose of LA was 1.0 g/kg/day and CA was 2.0 g/kg/day for 24 weeks. The serum phosphate was lower in the ADR-CA or ADR-LA group than in the ADR group and significantly lower in the ADR-CA group than in the ADR group at each point, but there were no significant differences between the ADR and ADR-LA groups. The serum phosphate was also lower in the ADR-CA group than in the ADR-LA group, and there was significant difference at week 8. The urinary phosphate was significantly lower in the ADR-CA group than in the ADR or ADR-LA group at each point. The urinary phosphate was also lower in the ADR-LA group than in the ADR group at each point, and significant difference at week 8. There were no significant differences in the serum creatinine or blood urea nitrogen among the three groups. In conclusion, this study indicated the phosphate-binding potency of LA isn’t twice as strong as CA, and neither LA nor CA suppressed the progression of chronic renal failure in the serum creatinine and blood urea nitrogen, compared to the untreated group.

Le degré de l’insuffisance rénale chronique est associé aux taux de cytokines pro-inflammatoires, à l’hyperhomocystéinémie et au stress oxydant

AimTo evaluate pro-inflammatory cytokines, homocysteinemia and markers of oxidative status in the course of chronic renal failure. Patients and methodsOne hundred and two patients (male/female: 38/64; age: 45±07 years) with chronic renal failure were divided into 4 groups according to the National Kidney Foundation classification. They included 28 primary stage renal failure patients, 28 moderate stage renal failure, 28 severe stage renal failure and 18 end stage renal failure. The inflammatory status was evaluated by the determination of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-1β, interleukin-6) and total homocysteine. Pro-oxidant status was assessed by assaying thiobarbituric acid reactive substances, hydroperoxides, and protein carbonyls. Antioxidant defence was performed by analysis of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase. ResultsInflammatory markers were elevated in the end stage renal failure group compared to the other groups (P<0.001). Indeed, an increase in thiobarbituric acid reactive substances, hydroperoxides and protein carbonyls was noted in the end stage renal failure group in comparison with the other groups (P<0.001), while the levels of antioxidants enzymes activity were decreased in the study population (P<0.001). ConclusionImpaired renal function is closely associated with the elevation of inflammatory markers leading to both increased markers of oxidative stress and decreased antioxidant defense.

Reply to “Letter to the Editor: ‘How does potassium supplementation lower blood pressure?’”

to the editor: We appreciate Dr. McDonough's and Dr. Nguyen's valuable comments and interest (6a) in our study. They raised several interesting issues regarding our recent paper ([4][1]), which explored the molecular mechanisms responsible for the blood pressure-lowering effect of potassium

Survival during renal replacement therapy of patients previously treated with a very low-protein diet supplemented with ketoacids : the Italian experience.

In the course of chronic renal failure, low protein-diets allow better control of metabolic disorders and may delay the start of renal replacement therapy (RRT). However, concerns exist that a very low protein diet supplemented with ketoacids (sVLPD) worsens survival after starting RRT. To evaluate whether a prolonged sVLPD regimen may affect all-cause mortality during the following RRT period, we studied time to all-cause death during RRT in patients previously followed in renal clinics either treated with sVLPD (sVLPD group, n =184, age 67±18 yrs) or not (CKD group, n =334, age 66±14 yrs). A Control group including 9,092 patients (age 66±14 yrs) was selected from the Italian dialysis & transplantation registry (RIDT). In sVLPD, CKD and Control groups, the prevalence of an history of cardiovascular disease was 41, 31, 25% and of diabetes was 18%, 31%, 17%, respectively; the median follow-up time in RRT (36, 32, 36 months) did not differ among groups.Cumulative survival was similar in sVLPD and CKD groups ( p =0.638), but significantly higher than in the Control group (Long-rank test, 20,62; p p =0.0001) in sVLPD and 0.65 [0.53−0.80] ( p =0.001) in CKD group. Due to age interaction with survival in sVLPD ( p =0.024), HRs for death reduced to 0.34 [0.16−0.73] and 0.58 [0.37−0.92] in sVLPD and CKD pts In conclusion, prescription of sVLPD during the conservative phase of chronic renal failure does not worsen, or even improves, survival after starting RRT. This survival advantage is more evident in patients younger than 70 years.

The Regulation of Parathyroid Hormone Secretion and Synthesis

Secondary hyperparathyroidism classically appears during the course of chronic renal failure and sometimes after renal transplantation. Understanding the mechanisms by which parathyroid hormone (PTH) synthesis and secretion are normally regulated is important in devising methods to regulate overactivity and hyperplasia of the parathyroid gland after the onset of renal insufficiency. Rapid regulation of PTH secretion in response to variations in serum calcium is mediated by G-protein coupled, calcium-sensing receptors on parathyroid cells, whereas alterations in the stability of mRNA-encoding PTH by mRNA-binding proteins occur in response to prolonged changes in serum calcium. Independent of changes in intestinal calcium absorption and serum calcium, 1α,25-dihydroxyvitamin D also represses the transcription of PTH by associating with the vitamin D receptor, which heterodimerizes with retinoic acid X receptors to bind vitamin D-response elements within the PTH gene. 1α,25-Dihydroxyvitamin D additionally regulates the expression of calcium-sensing receptors to indirectly alter PTH secretion. In 2°HPT seen in renal failure, reduced concentrations of calcium-sensing and vitamin D receptors, and altered mRNA-binding protein activities within the parathyroid cell, increase PTH secretion in addition to the more widely recognized changes in serum calcium, phosphorus, and 1α,25-dihydroxyvitamin D. The treatment of secondary hyperparathyroidism by correction of serum calcium and phosphorus concentrations and the administration of vitamin D analogs and calcimimetic agents may be augmented in the future by agents that alter the stability of mRNA-encoding PTH.

Effect of Renal Transplantation on Visual Evoked Potential Abnormalities of Chronic Renal Failure

Background Cranial neuropathies including optic nerve involvement are well-known complications of chronic renal failure (CRF), but most clinicians often do not follow the progression of these damages during course of CRF or their reversibility after treatment. So, this study evaluates effects of renal transplantation on visual system functions using visual-evoked potentials (VEP). Methods and Materials Forty CRF transplantation candidates and 40 control healthy persons underwent VEP before transplantation. VEP was repeated 3 months later for patients who had successful grafts. Results None of recorded VEP changes were significant in our study, although the absolute number of normal parameters increased after transplantation. In patients who had less than 1 year duration of CRF, more positive changes were observed after transplantation ( p < .05). Conclusion Our study showed the VEP changes were not significant. This may have been due to the delay in transplantation. CRF duration had a significant effect on almost all parameters of VEP which means that the longer duration of CRF lead to a decreased probability of VEP changes to return to normal after transplantation.

Endothelial Dysfunction in Chronic Renal Failure

Cardiovascular disease is a very early phenomenon in the course of chronic renal failure, and increases continuously with decrease of renal function. Endothelial dysfunction seems to be a starting point in vascular changes leading to atherosclerosis and artery calcification. Endothelium, considered the largest organ in the body, has many functions. It senses mechanical and hormonal stimuli and in response the endothelial cells secrete a range of compounds which modulate vascular tone, coagulation, cell proliferation, and inflammation. The central role of endothelium in the development of vascular disease has led to identification of new relevant biomarkers and methods to estimate endothelial function and injury. Arterial stiffness, which is not an early phenomenon in endothelial dysfunction but a common complication of chronic renal failure may be evaluated through Pulse Wave Velocity and Augmentation Index obtained by pulse-wave analysis. Aortic stiffness is an independent predictor of cardiovascular morbidity and mortality in patients with hypertension. A new fascinating aspect of research in endothelial function is rising through the studies on endothelial progenitor cells. These are primitive bone marrow cells that have the ability to mature into endothelial cells and have a physiologic role in the repair of endothelial lesions.

Changes in the Sodium and Potassium Transporters in the Course of Chronic Renal Failure

Background: In chronic renal failure (CRF), residual nephrons can increase their excretion of sodium (Na) and potassium (K). However, the mechanisms of renal Na and K regulation in late-stage CRF have not been clearly investigated. Methods: We examined altered expression of major renal Na and K transporters in Sprague-Dawley rats at 4 and 12 weeks after a 5/6 nephrectomy. Results: CRF rats were azotemic and had gradually increased levels of urinary Na and K excretion over time. At 4 weeks, the abundance of Na-K-2Cl cotransporter (NKCC2), and Na-Cl cotransporter (NCC) in CRF rats increased significantly (477 and 222% of the control, respectively). In contrast, expression of NKCC2 and NCC decreased markedly at 12 weeks (55.4 and 30.8%, respectively). Expression of epithelial Na channel-α increased throughout the whole period. The abundance of renal outer medullary K-channel (ROMK) and Na-K-ATPase did not decrease at 4 weeks, but it was reduced at 12 weeks. Conclusion: We suggest that increased urinary Na excretion in late-stage CRF may be associated with decreased expression of renal Na transporters except ENaC compared to early-stage CRF, and that increased urinary K excretion in the late stage of CRF may not be related to expression of ROMK.

Melatonin ameliorates oxidative stress, inflammation, proteinuria, and progression of renal damage in rats with renal mass reduction

The progressive deterioration of renal function and structure resulting from renal mass reduction are mediated by a variety of mechanisms, including oxidative stress and inflammation. Melatonin, the major product of the pineal gland, has potent_antioxidant and anti-inflammatory properties, and its production is impaired in chronic renal failure. We therefore investigated if melatonin treatment would modify the course of chronic renal failure in the remnant kidney model. We studied rats followed 12 wk after renal ablation untreated (Nx group, n = 7) and treated with melatonin administered in the drinking water (10 mg/100 ml) (Nx + MEL group, n = 8). Sham-operated rats (n = 10) were used as controls. Melatonin administration increased 13-15 times the endogenous hormone levels. Rats in the Nx + MEL group had reduced oxidative stress (malondialdehyde levels in plasma and in the remnant kidney as well as nitrotyrosine renal abundance) and renal inflammation (p65 nuclear factor-kappaB-positive renal interstitial cells and infiltration of lymphocytes and macrophages). Collagen, alpha-smooth muscle actin, and transforming growth factor-beta renal abundance were all increased in the remnant kidney of the untreated rats and were reduced significantly by melatonin treatment. Deterioration of renal function (plasma creatinine and proteinuria) and structure (glomerulosclerosis and tubulointerstitial damage) resulting from renal ablation were ameliorated significantly with melatonin treatment. In conclusion, melatonin administration improves the course of chronic renal failure in rats with renal mass reduction. Further studies are necessary to define the potential usefulness of this treatment in other animal models and in patients with chronic renal disease.

Decreased IL-10 mRNA expression in patients with advanced renal failure undergoing conservative treatment

Chronic renal failure (CRF) is characterized by persistent systemic inflammatory response. We tested the hypothesis that the balance between synthetic capacity of pro-inflammatory, as tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, and anti-inflammatory cytokines, as IL-10, may become progressively impaired during decline of renal function. Cytokine mRNA transcript levels (fraction of GAPDH mRNA) were detected by real time RT-PCR technique in whole blood cells of patients with far-advanced or less-advanced CRF (glomerular filtration rate lower or greater than 15 ml/min per 1.73 m 2, respectively) undergoing conservative treatment and in healthy controls. TNF-alpha mRNA levels were greater ( p < 0.05) in the patients with far-advanced CRF than in those with less-advanced CRF. IL-6 mRNA levels were not significantly different in the two groups. Both groups of patients exhibited greater ( p < 0.05) TNF-alpha and IL-6 mRNA levels than the healthy controls. IL-10 mRNA levels were greater ( p < 0.05) in the patients with less-advanced CRF (65 ± 18) than in the healthy controls (12 ± 2). Nonetheless, in the patients with far-advanced CRF, IL-10 mRNA levels (20 ± 10) were lower ( p < 0.05) than in the patients with less-advanced CRF and not significantly different than in the healthy controls. In conclusion, advanced renal failure is characterized by unbalanced synthetic capacity of pro- and anti-inflammatory cytokines. A progressive decrease in IL-10 synthetic capacity during the course of CRF could contribute to increasing cardiovascular risk.

Mathematical modelling of the course of chronic renal failure

Mathematical modelling of the course of chronic renal failure

Nutrition perdialytique

Malnutrition is frequent in course of chronic renal failure. More than 50% of patients with dialysis have clinical or biochemical signs of malnutrition. And malnutrition is an independent prognostic factor of long term mortality. Increasing caloric and proteic requirements, and decreasing oral intakes, are main components of malnutrition pathophysiology in chronic renal failure patients. Perdialytic parenteral nutrition could improved nutritional status but its effects on morbidity and mortality have to be demonstrated.

Serum VCAM-1, ICAM-1, and L-selectin levels in children and young adults with chronic renal failure

Children and young adults with chronic renal failure (CRF) present with an impaired immune response. Our aim was to analyze whether leukocyte migration, determined by adhesion molecules, is disturbed in the course of CRF, hemodialysis (HD), and peritoneal dialysis (PD). Soluble (s) VCAM-1, ICAM-1, and L-selectin serum levels were evaluated by ELISA in 15 patients with CRF, 22 patients on cuprophane membrane HD, 24 patients on PD, and in 15 controls. The sVCAM-1 levels in all groups were significantly elevated compared with controls. The levels in HD patients were higher than in CRF patients (P<0.05), while levels in PD patients were higher than in CRF and HD (P<0.001 and P<0.01, respectively). The sICAM-1 concentrations in CRF and PD patients were significantly elevated compared with controls (P<0.001 and P<0.0001, respectively); in PD patients sICAM-1 levels were higher than in HD patients (P<0.001), but there were no differences between other groups. sL-selectin levels were decreased in all groups compared with controls. The levels in HD patients were the lowest and the differences, compared with CRF and PD patients, were significant (P<0.05 and P<0.01, respectively). Children and young adults with CRF and on maintenance dialysis have altered concentrations of soluble adhesion molecules, resulting from either inadequate clearance or disturbed synthesis and release. The differences in sVCAM-1 levels between CRF and both groups of patients on dialysis, as well as the differences in sL-selectin concentrations between HD and CRF patients, indicate that these disturbances are aggravated by maintenance dialysis, particularly HD.

Features of the course of chronic renal failure in patients with diabetes mellitus who were on hemodialysis

То enhance the efficiency of treatment of patients with diabetic nephropathy, to prolong survival, and to improve life quality in them, the specific features of the clinical cause and the pattern of morbidity, the authors studied 28 patients with diabetes mellitus and the priority factors aggravating the course of diabetic nephropathy during renal replacement therapy. Their experience in treating patients with diabetes mellitus with programmed hemodialysis and peritoneal dialysis was analyzed. Cardiovascular diseases, the dyslipidemic syndrome that signals about progressive atherosclerosis of the aorta and coronary arteries rank first among a diversity of factors that aggravate prognosis, deteriorate life quality in patients with diabetic nephropathy, and promote the development of a fatal outcome. Hyper-(f-microglobulia develops along with dialysis amyloidosis. Immunity tension decreases and infectious complications develop in the respiratory and gastrointestinal tract. Cardiovascular diseases in patients with diabetic nephropathy are poor factors leading to sudden coronary death in severe cases. An individual approach to treating patients with diabetes mellitus complicated by nephropathy resulting in chronic renal failure makes it possible to optimize the success rates of programmed hemodialysis or peritoneal dialysis and to prolong their life span by 4-5 years.

Early referral to a nephrologist is associated with better outcomes in type 2 diabetes patients with end-stage renal disease

End-stage renal disease (ESRD) requiring renal replacement therapy (RRT) is a late complication of type 2 diabetes. The correlation between pre-ESRD medical care and outcome has been rarely studied in France. Community-based study of case-incIdent ESRD patients. Medical care practices were described retrospectively when starting RRT. Medical status, mortality, morbIdity, and quality-of-life were recorded prospectively. One hundred and fourty-eight ESRD patients with type 2 diabetes were included. Factors independently correlated with mortality within 3 Months of RRT onset were presence of physical impairment of ambulation at onset of RRT [odd ratio (OR): 5, (95%CI: 1.9-13.3)], and starting RRT in life-threatening circumstances [OR: 3.6, (95%CI: 1.2-10.7)]. Factors independently correlated with "poor outcome" 1 Year after the onset of RRT were BMI less than 20 kg/m2 [OR: 13.4, (95%CI: 1.5-120.2)] and presence of 2 [OR: 2.7, (95%CI: 0.9-8.4)], or 3 or more comorbId conditions [OR: 4, (95% CI: 1.4-11)]. Three Months after the first RRT session, survival was 16.4% better for patients who had had regular nephrological care versus none, and 9.1% better for those who had had late nephrological care versus none. Type 2 diabetes patients starting RRT in an emergency setting had had significant less regular nephrological care. Length of their first hospital stay was significantly longer. They were more likely to have lower resIdual renal function, gastrointestinal symptoms, lower serum albumin, lower hematocrit, lower serum calcium, and higher serum phosphorus. During the course of chronic renal failure in type 2 diabetes patients, early implementation of nephrological well-established guIdelines is associated with better outcome after starting RRT.