Studies   indicate that chronic pain is referred by chronicrenal patients with varying intensity, which induces the use of analgesics and consequent polypharmacy. The presence of pain brings as a consequence the reduction of physical function , changes in the sleep pattern  , depressive symptoms, and hindering of the quality of life  . Despite these limitations, it is a little valued symptom, in detriment to other priorities related to treatment , or under notified due to recognition and ap- propriate management barriers such as time limitations for assessing the patient, un- availability of evaluation instruments, lack of experience on the part of the professional, or belief that chronic pain is more difficult to be evaluated and handled .
In our study, patients only on conservative management were studied. This is because thyroid profile undergoes changes due to dialysis independent of that due to chronicrenal failure. Dialysis also changes the previous serum status of thyroid hormone in the patients with renal failure. Many studies have conducted by comparing CRF patients conservative Management and Hemodialysis by Ramirez 42
Chronicrenal failure refers an irreversible deterioration in renal function which classically develops over a period of years. Initially it is manifest only as a biochemical abnormality, eventually loss of the excretory metabolic and endocrine functions of the kidney leads to the development of the clinical symptoms and signs of renal failure, which is referred to as uremia. When death is likely without renal replacement therapy it is called end stage renal failure [ESRF] 
India, estimated a prevalence of chronicrenal failure of 0.16 per cent in the community in 2003; applying the Modification in Diet in Renal Disease (MDRD) equation for GFR estimation in 2005, 0.86 per cent was found to have a GFR 1.8 mg/dl. Estimates for the United States (US) population extrapolated from the National Health and Nutrition Examination Survey (NHANES III) data place the prevalence of CKD stages 4 and 5 (severe decrease in GFR) and CKD stage 3 (moderate decrease in GFR) at 0.4 percent. However, such direct comparisons with Western populations are not valid; since the equivalent GFR for a serum creatinine of 1.8 mg/dl in Indians may place the individual anywhere between CKD stages 2 to 4 depending upon gender and nutritional status. Modi and Jha reported from an urban population in the city of Bhopal, that the crude and age adjusted incidence rates of end stage renal disease (ESRD) were 151 and 232 per million population, respectively.
turnover rate, an abnormal accumulation of biologically inactive lipid-soluble metabolites, and the urinary excretion of both vitamin D 3 - 3 H and biologically inactive metabolites. Neither alterations in water-soluble vitamin D 3 metabolites nor qualitative abnormalities in protein-binding of vitamin D 3 were observed in the uremic subjects. Although hemodialysis proved ineffectual in reversing the observed abnormalities in vitamin D 3 metabolism and excretion, renal homotransplantation was completely successful in this regard. These experiments support the conclusion that the resistance to therapeutic doses of vitamin D often seen in patients with chronicrenal failure and renal osteodystrophy results from an acquired defect in the metabolism and excretion of vitamin D.
Chronicrenal disease (CRD) is generally thought to be incur- able, except through renal transplantation, and the number of patients with CRD is on the increase. Glomerulosclerosis and tubulointerstitial fibrosis represent the morphological equivalent of end-stage CRD. In this study, we demon- strated the preventive effect of hepatocyte growth factor (HGF) on the progression of renal dysfunction and fibrosis, using a spontaneous mouse model for CRD (ICGN strain). The mice progressively developed glomerular sclerotic in- jury, tubular atrophy, and renal dysfunction until they were 17 wk of age. When recombinant HGF was injected into these mice during a 4-wk-period (from weeks 14–17 after birth), DNA synthesis of tubular epithelial cells was found to be 4.4-fold higher than in mice without HGF injection, thereby suggesting tubular parenchymal expansion pro- moted by HGF. Notably, HGF suppressed the expression of transforming growth factor- b and of platelet-derived growth factor as well as myofibroblast formation in the af- fected kidney. Consequently, the onset of tubulointerstitial fibrosis was almost completely inhibited by HGF, while HGF attenuated the progression of glomerulosclerosis, both leading to preventing manifestation of renal dysfunction. From our results, supplement therapy with HGF may be taken into consideration as a novel option for prevention and treatment of CRD. ( J. Clin. Invest. 1998. 101:1827– 1834.) Key words: chronicrenal failure • HGF therapy •
It may cause, as well as be a consequence of chronicrenal disease. Previously it was thought that hypotension leads to glomerular sclerosis due to ischaemia where there was decreased glomenmlar perfusion resulting from renal vascular disease. More recent data has suggested that glomerular sclerosis could occur in the absence of arteriosclerotic disease and in many cases glomerular capillary hyperper fusion and hypertension could initiate glomemlar structural injury 19 . Systemic hypertension is not required for the development of glomerular capillary hyper filtration and hypertension. In diabetic rats a pathological reduction in afferent arteriolar resistance leads to an increase inglomemlarcapillary flow and allows a greater fraction of systemic blood pressure to be transmitted into the glomerular capillary network. This raises the glomerular capillary hydraulic pressure inspite of normal renal perfusion pressure 20,21 . Systemic blood pressure tends not to decline with protein rcstriction but glomerular injury is arrested 22,16 ; this emphasizes the importance of glomerular than systemic haemodynamics. Studies have also shown that it is glomerular capillary hypertension rather than hyperfiltration or hyperperfusion which is the critical detenninant of glomerular cell injury. Thus control of glomerular capillary pressure may concur renal protection even in the lace of the continued systemic hypertension. The factors that increase glomemlar capillary hydraulic pressure experimentally were: a high protein diet, dietary cholesterol supplementation 27 , administration of glucocorticoids 28 , minerallocorticoids 29,30 or erythropoitin 31 . There arc various studies %vhich defined the role of angiotensin converting enzymes inhibitors in not only controlling blood pressure but also limiting proteinurea and slowing development of glomerular sclerosis in experimental models. ACE inhibitors normalized both systemic and glomerular capillary pressure 32-37 and thereby they are most consistently beneficial in slowing progression of experimental renal disease. The role of calcium channel blocker 5 is still under study and various studies have shown conflicting result of this family of drugs 38-44 . Several other drugs like a diuretic, vasodilator or centrally acting agent or a combination of the three have also been used though there have been very good control of blood pressure with the above drugs. Renal protection has been quite variabic with this regimen 45 . Beta adrenergic blockers have also been studied widely but the results available are not very encouraging. The deleterious consequences of intra- glomemlar hypertension besides its direct destmctive effect, have been suspected to be due to glomerular endothelial damage. This in turn may precipitate intra-glomerular coagulation 46 and increase the mesangial "trafficking" of macromolecules which promote glomemlosclerosis 46 Role of Dietary Proteins
simultaneous renal clearance of ordinary urea, which averaged 2.0 liters/day. The difference, extrarenal clearance of urea, averaged 3.1 liters/day as compared with a previously reported mean of 18 liters/day in normal subjects. Thus urea-splitting activity in the gut of uremic subjects expressed in these terms is far less than in normal individuals. Nevertheless, the amount of ammonia N formed from urea in these patients, 3.5 g/day, is not significantly different from normal, owing to their elevated plasma urea. In the same
administered, as there is impaired adrenal reserve in profound hypothyroidism. Any precipitating factors should be treated, including the early use of broad-spectrum antibiotics, pending the exclusion of infection. Ventilatory support with regular blood gas analysis is usually needed during the first 48 h. Hypertonic saline or intravenous glucose may be needed if there is severe hyponatremia or hypoglycemia; hypotonic intravenous fluids should be avoided because they may exacerbate water retention secondary to reduced renal perfusion and inappropriate vasopressin secretion. The metabolism of most medications is impaired, and sedatives should be avoided if possible or used in reduced doses. Medication blood levels should be monitored, when available, to guide dosage
Hypotheses to explain these epidemiological changes in 10 years are numerous: a methodological bias when the stage of kidney disease is defined by a single sampling of the serum creatinine , high mortality in CKD patients aged over 70 years, 52% of patients with stage 3-4 renal disease and aged over 70 years dying before ESRD treatment , a support increasingly early in replacement therapy as shown by serum creatinine at the time of dialysis that happened in the USA, from 87 mg / l in 1995 to 67 mg / l in 2004 .
Unlike acute renal failure, chronicrenal failure represents progressive and irreversible destruction of kidney structures. Many patients with chronicrenal failure progressed to the final stages of the disease and then died. The high mortality rate was associated with limitations in the treatment of renal disease and with the tremendous cost of ongoing treatment. In the United States, there are approximately 400,000 persons with end-stage renal disease who are living today, a product of continued research and advances in treatment renal failure can result from many conditions that cause permanent loss of nephrons, including diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. Typically, the signs and symptoms of renal failure occur gradually and do not become evident until the disease is far advanced. This is because of the amazing compensatory ability of the kidneys. As kidney structures are destroyed, the remaining nephrons undergo structural and functional hypertrophy, each increasing its function as a means of compensating for those that have been lost. It is only when the few remaining nephrons are destroyed that the manifestations of renal failure become evident. 
chronicrenal disease, chronic liver disease, diabetes mel- litus, cancer, autoimmune disease, human immunodefi- ciency virus (HIV) infection, and 'other chronic diseases'. Alcoholism was defined as known abuse. Smoking was considered in two categories: never or ever. Results of chest roentgenograms were obtained and the presence of pulmonary infiltrates or pleural effusions noted.
Eighty-eight healthy Saudi females were recruited from an endocrine clinic in a tertiary care hospital in southern region of Saudi Arabia. History taking and clinical examination were done for all participants. All were females within the age range of 18 to 50 years. Diabetes mellitus, Chronicrenal impairment, chronic liver disease, other chronic illnesses, anemia, pregnancy, lactation and intake of medications that may affect vitamin D3 level, plasma glucose, HbA1c or lipid profile lead to exclusion from the study.
Anaesthetists need a working understanding of the implications of renal impairment for the safe conduct of anaesthesia. Patients with renal failure are often encountered when managing elective or emergency surgical cases. In addition, it is fundamental to consider how kidney injury frequently forms part of the clinical picture during resuscitation and optimisation of acutely unwell patients in the emergency department or critical care. The functions of the kidney are multiple, and beyond the scope of this paper. The aim of this review is to summarise current classifications of renal impairment and explore the evidence underpinning relevant practice in anaesthesia. Patient groups include those with chronicrenal failure, patients with acute renal failure, and also patients with normal preoperative renal function but who have a high risk of developing peri-operative kidney injury. There is a dearth of strong evidence to guide anaesthetic practice with regards to renal failure. As a result, many of the studies quoted here are small cohorts, case series, or case reports. In general, anaesthetists are still mainly guided by their knowledge of physiology, pharmacology
Methods: We performed a cross-sectional study of 3599 patients with chronic kidney disease enrolled in the ChronicRenal Insufficiency Cohort (CRIC) study. All subjects were asked to complete the Modification of Diet in Renal Disease (MDRD) study patient symptom form. Our main predictor is GI symptom score. Serum level of C-reactive protein (CRP) was measured as well. Main outcome measures are serum albumin levels and prevalence of hypoalbuminemia. Results: Of the participants assessed, mean serum albumin was 3.95 ± 0.46 g/dL; 12.7 % had hypoalbuminemia. Patients with lower estimated glomerular filtration rate (eGFR) were likely to have more GI symptoms (apparent at an eGFR <45 ml/min/1.73 m 2 ). Patients with worse GI symptoms had lower dietary protein intake. GI symptoms, like inflammation, were risk factors for lower serum albumin levels. However, adding GI symptom score or CRP into the multivariable regression analysis, did not attenuate the association between lower eGFR and lower albumin or hypoalbuminemia.
Chronicrenal failure was the cause of 33 cases of CCF. These were mainly due to chronic hypertensive nephrosclerosis. This consisted of 23 (69.8%) males and 10 (30.2%) females. Four patients had thyrotoxic heart failure with a patient presenting with heart failure due to ischemic heart disease. The causes of CCF in 47 (11.1%) patients could not be ascertained from the records. Of the total number of patients with clinical features of CCF, 408 had chest X-ray, 312 had resting ECG, while only 146 had echocardiography.