Type 2 diabetes end stage renal disease,diabetic weight loss cleanse tea,diab?te de type 2 pr?vention jeunesse,medical management of diabetes mellitus in pregnancy pdf - PDF Review

In contrast to Type 1 diabetes mellitus (DM), the incidence of non-diabetic renal disease (NDRD) is very high in Type 2 diabetic patients. It is now accepted that clinical nephropathy (proteinuria) in Type 2 diabetic patients may be histologically associated with the development of diabetic glomerulopathy or non-diabetic renal disease or both. There is abundant evidence that the risk to develop proteinuria and renal failure is similar for patients with Type 1 or Type 2 diabetes (Figures 1 and 2). The majority of patients whose history and clinical findings are compatible with diabetic kidney disease do not benefit from kidney biopsy, because the diagnosis is usually not altered. Criteria for renal biopsy in proteinuric Type 2 diabetes mellitus patients have not been defined.
It is well-known that diabetic nephropathy (DN) occurs in more than 95% of patients having Type 1 diabetes for more than 10 years, whereas non-diabetic nephropathy is rare, accounting for 2-3% of unselected Type 1 diabetic patients with proteinuria.
A 46 year old male detected to have Type 2 DM 03 years ago presented with swelling over legs of 9 months duration. We have observed remission of massive proteinuria and complete reversal of Acute Renal Failure (ARF) in Type 2 diabetic patients with histological diagnosis of chronic interstitial nephritis with minimal change disease treated with steroid (case 2). A 45 year old gentleman known diabetic and hypertensive since February 2004 was admitted on 27th February 2009 with complaint of swelling of both legs for 5 months as well as decreased urine output, nausea and breathlessness for 10 days. In addition, symptomatic treatment for fluid and salt retention (diuretic and salt restriction), antihypertensive drugs for control of blood pressure and non-specific measures like ACEi and ARB may be required for control of proteinuria. The treatment options for diabetic ESRD are; (i) Haemodialysis, (ii) Continuous Ambulatory Peritoneal Dialysis (CAPD) and (iii) Renal transplantation. All clinical nephropathies (proteinuria, increased creatinine) in Type 2 DM are not due to diabetic nephropathy.
Calciphylaxis causes calcification, thrombosis, cutaneous ischemia, and necrosis in the skin and subcutaneous tissue. Calciphylaxis is a syndrome of vascular calcification, thrombosis, cutaneous ischemia, and necrosis (1). Whether calciphylaxis is a systemic process or is confined to the skin and subcutaneous tissue is unknown, since no formal studies have addressed this question.
For the purposes of this study, we defined calciphylaxis as the clinical findings of indurated patches with ischemia or infarction and ulceration, with supportive histopathologic findings of tissue ischemia and necrosis due to arteriolar calcification, extravascular calcification, intimal fibroplasia, and thrombosis (1).
Antemortem skin biopsies substantiated a clinical diagnosis of calciphylaxis in all 3 patients (Fig. The autopsy reports indicated that all 3 patients had histopathologic evidence of cardiovascular calcification (Fig. Thus, although vessel calcification was identified in other organs, other microscopic features of calciphylaxis were not reported to be present in organs other than the skin. The histopathologic diagnosis of calciphylaxis in any organ system requires the presence not only of vascular and tissue calcification but also of associated tissue necrosis. We chose to study the autopsy data from these patients because postmortem examination is more thorough and systematic than antemortem physical examination, biopsy findings, or imaging studies.
Other reports have noted a€?visceral calciphylaxisa€? in patients on whom an autopsy was not performed or reported (9, 10).
We acknowledge the limitations of this review, including its retrospective design, the small number of patients with calciphylaxis who had autopsy and thus met inclusion criteria, and the possible selection bias of including only those patients on whom an autopsy had been performed.
We conclude that in the study population, calciphylaxis was a cutaneous process alone and did not involve other organs. Metabolic diseases, inherited: Also called inborn errors of metabolism, these are heritable (genetic) disorders of biochemistry. Markers of kidney damage in addition to proteinuria include abnormalities in the urine sediment and abnormalities on imaging studies. Urine sediment examination or dipstick for red blood cells and white blood cells should be performed in patients with chronic kidney disease and in individuals at increased risk of developing chronic kidney disease.
Imaging studies of the kidneys should be performed in patients with chronic kidney disease and in selected individuals at increased risk of developing chronic kidney disease. Although several novel urinary markers (such as tubular or low-molecular weight proteins and specific mononuclear cells) show promise of future utility, they should not be used for clinical decision-making at present. Abnormal urinary excretion of albumin and total protein (Guideline 5) is a highly sensitive indicator of glomerular disease. In some specific types of chronic kidney disease, abnormalities other than proteinuria are present prior to reduction in GFR.
Examination of the urinary sediment, especially in conjunction with assessment of proteinuria, is useful in the detection of chronic kidney disease and in the identification of the type of kidney disease.
Cells may originate from the kidneys or from elsewhere in the urinary tract, including the external genitalia. The presence of formed elements in the urinary sediment may indicate glomerular, tubulointerstitial, or vascular kidney disease. Urine dipsticks include reagent pads that are sensitive for the detection of red blood cells (hemoglobin), neutrophils and eosinophils (leukocyte esterase), and bacteria (nitrites).
Hydronephrosis on ultrasound examination may be found in patients with urinary tract obstruction or with vesico-ureteral reflux. Some constellations of abnormalities in blood and urine tests or imaging studies comprise specific clinical presentations of kidney disease. Decreased GFR and kidney failure are markers of more severe kidney disease (CKD Stages 2 through 5). Increased urinary excretion of some low molecular weight (LMW) proteins and N-acetyl--D-glucosaminidase (NAG) are key diagnostic indicators in a number of specific tubular diseases and may identify patients at higher risk of GFR decline in other kidney diseases (Tables 66, 67, 68, and 69) (C). In adult patients with either clinically stable systemic lupus erythematosus (SLE) nephritis (WHO classes IIIa, b, IVb, c) or clinically active SLE nephritis (WHO classes IVb, c), only the patients with active disease showed evidence of podocyturia.242 In adult patients with type 2 diabetes, podocytes were present in the urine of 53% of microalbuminuric subjects and 80% of macroalbuminuric subjects, but in none of the normoalbuminuric subjects.
The findings of hematuria, pyuria, and casts on urinalysis, or of cystic or echogenic kidneys on ultrasound, are well established as indicators of various chronic kidney diseases. In patients known to have chronic kidney disease on the basis of a decreased GFR, urinalysis and imaging studies may yield important diagnostic information. In patients not previously known to have chronic kidney disease but presenting with symptoms suggestive of kidney disease (eg, edema, hematuria, or flank pain), examination of the urinary sediment may confirm the presence of kidney disease. Examination of the urinary sediment may lead to the detection of kidney disease in patients presenting for evaluation of symptoms related to other organ systems.
In selected individuals with a normal GFR, but known to be at risk of chronic kidney disease, markers may serve as screening tests.
Application of the newer urinary markers (mononuclear cells and specific proteins such as NAG) described herein must await their validation in more extensive clinical studies. Novel and expanded uses of established methodologies (such as Doppler or functional MRI) should be pursued in clinical research studies. A wide spectrum of non-diabetic nephropathy (NDN) including both glomerular and tubulointerstitial lesions are reported in patients with Type 2 DM and their precise diagnosis requires histological examination of kidney tissue. Type 2 DM accounts for about 90% of all cases of diabetes and its incidence is rapidly increasing particularly in developing countries. It has been reported that 12-80% of Type 2 diabetic patients with renal involvement show non-diabetic renal disease.6-10 The large variation reported in these studies may be due to selection bias because renal biopsies were performed in those with clinically atypical diabetic nephropathy.
NDRD is a common feature in patients with Type 2 diabetes and has significant impact on prognosis and treatment which are different from DN.5,6,7 Renal biopsy is necessary to diagnose NDRD.
However, several analyses have shown 20-30% of Type 2 diabetic patients with ESRD suffer from primary chronic renal disease such as polycystic kidney disease, analgesic nephropathy, glomerulonephritis and ischemic nephropathy (Table 2). However, the incidence of ESRD in diabetic patients has increased dramatically in the past decades and majority of diabetic ESRD patients have Type 2 diabetes mellitus. However, diabetic patients are not immune to the renal lesions other than diabetic nephropathy. However, renal biopsy is helpful in diagnosis of certain treatable non-diabetic renal diseases in Type 2 diabetic patients. Usually, criteria for renal biopsy in Type 1 DM are used (duration of diabetes < 5 years, microhematuria, absence of diabetic retinopathy, uncharacteristic changes in renal function or immunological abnormalities). He denied family history of diabetes, hematuria, peripheral neuropathy or systemic illness.
There is no doubt that kidney transplantation particularly combined with pancreas transplantation, provides optimal survival and the best quality of life. One should be aware of non-diabetic renal diseases in proteinuric Type 2 diabetic patients. Clinical identification of non-diabetic renal disease in diabetic patients with Type I and II disease presenting with renal dysfunction. Increased prevalence of renal biopsy findings other than diabetic glomerulopathy in Type-II diabetes mellitus. Renal affection in patients with diabetes mellitus is not always caused by diabetic nephropathy (Abstract). Renal pathological change in patients with Type 2 diabetes is not always diabetic nephropathy : A report of 52 cases. Diabetic retinopathy is a poor predictor of type of nephropathy in proteinuric Type 2 diabetic patients. More than one-third of Type 2 diabetic with renal diseases do not have diabetic retinopathy : A prospective study (Abstract).
Idiopathic membranous glomerulonephritis in diabetic patients : Reporting three cases and review of the literature. Association of diabetic retinopathy and renal function in patients with Type 1 and 2 diabetes mellitus. Prevalence of micro and macro albuminuria, arterial hypertension, retinopathy and large vessel disease in European Type 2 (NIDDM) diabetic patients. Nephrotic syndrome in patients with diabetes mellitus is not always associated with diabetic nephropathy. Calciphylaxis has been reported anecdotally to affect visceral organs in the setting of cutaneous calciphylaxis (6a€“10). Patients were excluded if they had denied research authorization or did not meet inclusion criteria.
Anatomic distribution of calciphylaxis was reported on autopsy as involving upper extremity (n = 1), torso (n = 1), and lower extremity (n = 3).
Other findings, such as vascular occlusion by thrombi and intraluminal fibrosis, may support the diagnosis. Scattered case reports have reported autopsy findings in patients with calciphylaxis (Table III) (6a€“8, 11a€“21).

These patients had antemortem bio­psies from extracutaneous organs that showed findings said to be consistent with calciphylaxis in the lungs and gastrointestinal tract. The term was coined by Hans Selye (22) in 1962 to describe skin necrosis that was provoked by exposure to substances such as parathyroid hormone and vitamin D, and it was associated with cutaneous calcification in experimental animals. Our study is of just 3 patients: further autopsy studies from patients with calciphylaxis are needed to confirm or refute our findings that calciphylaxis only involved skin and does not seem to involve extracutaneous organs. Examples include albinism, cystinuria (a cause of kidney stones), phenylketonuria (PKU), and some forms of gout, sun sensitivity, and thyroid disease. Constellations of markers define clinical presentations for some types of chronic kidney disease. The results of urine sediment examination and of imaging studies of the kidney, however, can also suggest other types of chronic kidney diseases, including vascular, tubulointerstitial, and cystic diseases of the kidney. In general, urinalysis and ultrasound of the kidneys are helpful non-invasive tests to detect kidney damage.
Urinary sediment examination is recommended in patients with chronic kidney disease and should be considered individuals at increased risk of developing chronic kidney disease. Casts form only in the kidneys and result from gelation within the tubules of Tamm-Horsfall protein, a high molecular weight glycoprotein derived from the epithelial surface of the distal nephron. Significant numbers of erythrocytes, leukocytes, or cellular casts in urinary sediment suggest the presence of acute or chronic kidney disease requiring further work-up. Thus, urine sediment examination is generally not necessary for detection of these formed elements.
Imaging studies are recommended in patients with chronic kidney disease and in patients at increased risk of developing chronic kidney disease due to urinary tract stones, infections, obstruction, vesico-ureteral reflux, or polycystic kidney disease. The other presentations can occur without decreased GFR (CKD Stage 1) and can therefore serve as markers of kidney disease. There are disorders resulting from abnormal tubule handling of water or solutes, without decreased GFR. Most kidney diseases are asymptomatic, but in some tubulointerstitial diseases symptoms are associated with the kidneys or lower urinary tract. Abnormalities in urinary protein excretion or in urinary sediment without decreased GFR or urinary tract symptoms. These include structural abnormalities of the kidney observed on imaging studies, without decreased GFR, urinary tract symptoms, or abnormal urinalysis.
Sustained elevation of arterial blood pressure as the result of disease of the parenchyma or major vessels of the kidney, with or without decreased GFR, but usually with either urinary abnormalities or radiologic abnormalities. In the proper setting, these findings are sensitive markers for the presence of chronic kidney disease, although they may not suggest a specific diagnosis. For example, the finding of red blood cell casts in the urine indicates a high likelihood of a proliferative glomerulonephritis.
Abnormalities in the sediment will be present in a large proportion of patients with chronic kidney disease. The evaluation of the urine in patients with signs of vasculitis or with carcinomas may result in detection of associated kidney disease. For example, a patient at risk on the basis of a positive family history of polycystic kidney disease should undergo a screening kidney ultrasound one or more times before adulthood.
Several novel urinary markers show promise of noninvasive demonstration of kidney damage or prediction of disease progression. Renal biopsy studies suggest that 25-50% of patients with Type 2 diabetes had glomerular lesions unrelated to or in addition to diabetic nephropathy. Diabetes specific renal disease (Diabetic nephropathy) develops in about one-third of all people with Type 1 or Type 2 diabetes and it contributes to about 30% of end-stage renal disease (ESRD) in various countries.
However, it is generally agreed that renal biopsy cannot be used as a routine diagnostic test in Type 2 diabetic patients with proteinuria. The major reason for the apparent increase in the number of patients with Type 2 diabetes and ESRD is the progressive diminution of cardiac mortality in these patients and now-a-days such patients survive long enough to experience advanced nephropathy and ESRD.22 However, it is obvious that ESRD in Type 2 diabetic patients is not always associated with diabetic nephropathy (Table 2). Indeed, it may be possible that the abnormal diabetic kidney is more susceptible to different types of glomerulonephritis. DGS is the most commonly found renal lesions in Type 2 DM patients with proteinuria biopsied according to T1DM criteria even in presence of microhematuria or absence of retinopathy. From clinical point of view, the majority of patients with diabetic renal disease have retinopathy; however, the reverse is not true. In the light of the high prevalence of NDRD, it is appropriate for performing renal biopsy in Type 2 diabetic patients with clinical suspicion of NDRD; especially with overt proteinuria with or without retinopathy.
The combined kidney and pancreas transplantation is certainly optimum procedure for young person with Type 1 DM, if transplantation is performed in older people with Type 2 diabetes, it is usually kidney transplant alone. Renal biopsy in Type 2 DM proteinuric patients using biopsy criteria in Type 1 DM is not useful in identifying patients with potentially treatable NDRD. To identify whether other organs are affected we reviewed pathology reports of patients with calciphylaxis who underwent autopsy at Mayo Clinic, Rochester, Minnesota, between January 1, 1970, and December 31, 2011.
Davis, MD, Department of Dermatology, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA. Affected patients have clinical findings of painful indurated subcutaneous patches with overlying violaceous ischemic or infarctive skin involvement that progress to ulceration. Microscopic examination of subcutaneous tissue of a patient with calciphylaxis (hematoxylin-and-eosin stain). In these cases, however, this conclusion rested on the presence of calcification of visceral blood vessels, a non-specific microscopic finding in patients with concomitant peripheral vascular disease. Two patients had been diagnosed with end-stage renal disease secondary to diabetes mellitus before developing calciphylaxis. Microscopic findings from autopsies (hematoxylin-and-eosin stain): (a) Aortic atherosclerosis, grade 1 (of 4), non-ulcerocalcific. Calcification in unusual anatomical locations or that it is extensive is insufficient for a diagnosis of systemic calciphylaxis.
The vast majority of the reports document vascular calcification but not calciphylaxis of these internal organs (defined as in methods); in only 2 case reports would criteria perhaps fit with these criteria.
In most of these cases, calcium deposition was noted systemically, but microscopic criteria that would satisfy a diagnosis of calciphylaxis were not described.
The pathogenic mechanism of calciphylaxis has since been likened to a€?the skin equivalent of a myocardial infarction,a€? since vessel narrowing by intravascular calcification and fibrosis leads to tissue ischemia after an acute event such as thrombo-occlusion (23).
These are only a very few of the hundreds of known inborn errors of metabolism. Advances in the diagnosis and treatment of inborn errors of metabolism have improved the outlook for many of these conditions so that early diagnosis, if possible in infancy, can be helpful. New markers are needed to detect kidney damage that occurs prior to a reduction in GFR in other types of chronic kidney diseases. In addition, proteins other than albumin in the urine may indicate tubulointerstitial injury. In addition, these assessments provide clues to the type (diagnosis) of chronic kidney disease. Casts entrap material contained within the tubular lumen at the time of cast formation, including cells, cellular debris, crystals, fat, and filtered proteins.
The differential diagnosis for persistent hematuria, for example, is quite broad, including glomerulonephritis, tubulointerstitial nephritis, vascular diseases, and urologic disorders. Increased cortical echoes are a nonspecific but sensitive indicator of glomerular, interstitial, or vascular diseases. Table 65 describes the most frequent presentations for each type of chronic kidney disease.
They include diverse disorders such as renal tubular acidosis, nephrogenic diabetes insipidus, hyporeninemic hypoaldosteronism and other potassium secretory defects, renal glycosuria, renal phosphaturia, renal aminoaciduria, and many others. Principal abnormalities include hematuria with red blood cell casts (due to glomerular diseases), pyuria with white blood cell casts, renal tubular cells, coarse granular casts, or non-nephrotic proteinuria.
Since the novel markers described above (eg, low molecular weight proteinuria, mononuclear cyturia) have only been correlated with various chronic kidney diseases in a few studies to date, their application in clinical practice has not been established. On ultrasound examination, the presence of a kidney stone and findings of obstruction may help to explain acute flank pain. Findings suggestive of kidney disease may be expected to occur frequently in the evaluation of individuals presenting with hypertension, especially younger individuals. Histological studies confirm that NDRD can occur in isolated form without diabetic nephropathy or superimposed on diabetic nephropathy. Therefore, it is very important to determine the clinical predictive factors for NDRD in Type 2 diabetic patients. The high incidence of ESRD in patients with Type 2 diabetes is particularly cause for concern, since medical rehabilitation, quality of life and survival are consistently worse in diabetic compared with non-diabetic dialysed patients. Renal lesions in Type 2 diabetes are much complex and differ in Type 2 and Type 1 diabetes. Thus, these biopsy criteria are not useful in identifying patients with potentially treatable other renal lesions in Type 2 diabetic patients. Hyperglycemia is the key initiating factors for development of microvascular complication of diabetes, and it takes years before complications such as retinopathy (RP) and nephropathy (NP) develops.
The kidney biopsy is helpful in two ways; (i) It will differentiate diabetic from non-diabetic glomerulopathy and (ii) Knowledge of the underlying cause of proteinuria, may play an important role in planning the correct treatment of these patients. It is obvious that complications of diabetes are much more common in patients with diabetes when they have diabetic nephropathy.
Unfortunately, because of limited availability of organs, the great majority of people with Type 2 diabetes are not given transplant but treated by either hemodialysis or CAPD. Microscopic findings include cutaneous ischemia and necrosis due to calcification, intimal fibroplasia, and thrombosis of pannicular arterioles (Fig.
Pertinent features include intraluminal and extravascular calcification, intimal fibrosis of vessel walls, fat necrosis, and vascular thrombosis. To investigate this question, we retrospectively reviewed the autopsy reports of patients at our institution with calciphylaxis to characterize extracutaneous findings related to vascular or tissue calcification or tissue ischemia. We reviewed all autopsy reports and microscopically examined representative archived tissue sections from extracutaneous organs reported to have calcification. Microscopic features of calciphylaxis are not present (b) Monkeberg medial calcification of a renal artery, with the changes of severe diabetic nephropathy, acute tubular injury, and mild interstitial chronic inflammation. One reported a€?extensive vascular calcium deposition within multiple mesenteric vessels in the small bowel, with full-thickness necrosis; also in the duraa€? (7), and another reported a€?diffuse medial calcification, with intimal fibrosis and cellular thickening, partly accompanied by microthrombi involving small- to medium-sized visceral arteriesa€? (8).
While vascular mural calcification is not sufficient for a diagnosis of calciphylaxis, mural calcifation does appear to be an early and essential process in the development of a calciphylaxis plaque.

Calciphylaxis in a patient with Crohna€™s disease in the absence of end-stage renal disease. At present, there are no clinically proven markers specific for tubulointerstitial or vascular diseases of the kidney.
Gelation of Tamm-Horsfall glycoprotein is enhanced in concentrated urine and at acidic pH levels. Therefore, as with proteinuria, specific diagnosis requires correlation of urinalysis findings with other clinical markers.
Imaging studies employing iodinated contrast agents can cause acute kidney damage and may present significant risks to some patients with decreased kidney function. Table 64 defines these presentations according to level of GFR, markers of kidney disease (urine protein excretion, urine sediment examination, imaging studies), and other clinical features. In particular, inasmuch as these markers may correlate strongly with proteinuria, it is not certain that they can yet be considered independent indicators of disease or predictors of risk of disease progression. The finding of diffuse nephrocalcinosis and nephrolithiasis on ultrasound in a patient with decreased GFR could suggest the possible diagnosis of hyperoxaluria, leading to specific blood tests. Radiologic assessment may help to clarify other aspects of the nature of the kidney involvement.
Longitudinal and follow-up studies are necessary to verify whether abnormal NAG and possibly retinol-binding protein excretion in normoalbuminuric diabetic patients reliably predict later development of microalbuminuria and diabetic nephropathy. Diabetic nephropathy can occur in absence of retinopathy and chance of getting diabetic and non-diabetic renal lesions are nearly equal in Type 2 diabetic patient in absence of diabetic retinopathy (RP). In contrast with Type 1 diabetes, the prevalence of NDRD in proteinuric Type 2 diabetic patients is very high. Further, early diagnosis of NDRD is crucial as appropriate therapy could prolong renal survival in this patient population.
Thus, in addition to specific measures directed at managing kidney failure, intensive effort must be directed at identification and management of these problems as listed in Table 5. The renal-retinal relationship is well established for the clinical diagnosis of diabetic nephropathy in Type 1 DM. We also reviewed the medical literature to identify additional reported autopsy findings in patients with calciphylaxis. The third patient received a diagnosis of calciphylaxis associated with metastatic cholangiocarcinoma without end-stage renal disease. Two patients had annular calcification of the heart valves (mitral [n = 2] and aortic [n = 1]).
Microscopic changes of calciphylaxis, including extravascular calcification, intramural thrombosis, and intimal fibrosis of the vessel walls, are not present.
Although intra- and extravascular calcium deposition was noted in other organs, associated tissue ischemia or necrosis (as required for calciphylaxis) was not reported. Without reviewing this reported pathology, it is difficult to confirm whether or not these findings truly represented calciphylaxis of these organs. In one postmortem study, an incisional skin biopsy specimen from a patient with calciphylaxis showed subcutaneous vascular mural calcification, extravascular calcification, which extended peripherally by as much as 3 cm, and thromboses within the dermis and subcutis (24).
The presence of red blood cell casts strongly suggests glomerulonephritis as the source of hematuria.
For example, bilateral small echogenic kidneys in a patient presenting with newly detected decreased kidney function can suggest a chronic rather than an acute process. Similar studies are needed to confirm whether increased -2-microglobulin excretion predicts development of kidney failure in patients with idiopathic membranous nephropathy.
The presence of RP suggests the concurrence of DN, but does not exclude non-diabetic nephropathy. The clues for NDRD in Type 2 diabetic patients are; (i) Nephrotic syndrome with normal renal function, (ii) Impaired renal function with no proteinuria, (iii) Absence of retinopathy, (iv) Sudden deterioration of renal function, (v) Active urinary sediment, (vi) Gross or microscopic hematuria, (vii) Short duration of diabetes. A wide spectrum of non-diabetic nephropathy (NDN) including both glomerular and tubulointestinal lesions are reported in patients with Type 2 DM and their precise diagnosis require histological examinations.
There was no evidence of diabetic retinopathy, systemic infection and obvious cause of AKI. Autopsy reports showed that despite evidence of vessel calcification elsewhere, there was no evidence of calciphylaxis in other organs.
Calciphylaxis has been reported most commonly in patients with dialysis-dependent renal failure, although it can occur in many other clinical settings (2a€“5).
The extracutaneous calcium deposition noted postmortem in these patients was related to comorbidities, including diabetes mellitus, atherosclerosis, and end-stage kidney disease. The choice of urine sediment examination versus dipstick depends on the type of kidney disease that is being considered.
Longitudinal studies of urinary excretion of specific cell types (macrophages, NK cells, podocytes) in diabetic nephropathy, Henoch-Schonlein nephropathy, and IgA nephropathy are also necessary in order to confirm preliminary findings that cyturia is strongly associated with activity in these diseases. Clearly, renal biopsy is indicated in proteinuric Type 2 diabetic patients for precise diagnosis of diabetic vs non-diabetic renal disease. Kidney biopsy was done and light microscopy revealed chronic TIN with Minimal Change Disease. The control of blood pressure is difficult, requiring multiple drugs in patients with diabetic ESRD. Biopsy proven DN have been reported to occur in proteinuric Type 2 diabetic patient in absence of retinopathy.
All patients had histopathologic evidence of cardiovascular calcification, and atherosclerosis of coronary arteries and aorta.
The prognosis is dismal for patients with calciphylaxis, with an estimated one-year survival of 45.8% (1). Therefore, although patients with calciphylaxis not surprisingly have systemic evidence of chronic vascular stress and injury, the pathophysiology of calciphylaxis appears to have been confined to the skin in these patients. Preliminary work on the urinary excretion of podocyte-specific marker proteins such as podocalyxin and nephrin should be validated by further studies. Remission of nephrotic syndrome was observed with prolonged (4-6 month) course of corticosteroid therapy in patients with FSGS in Type 2 proteinuric diabetic patients (case 1). The diabetic patients with renal failure carry the risk of hypoglycemia and use of metformin is associated with risk of lactic acidosis. Urinary eosinophils have been specifically associated with allergic tubulointerstitial nephritis. Table 63 provides a brief overview of possible interpretations of abnormalities on imaging studies of the kidney. His renal function gradually improved and he became dialysis independent in April 2009 (Blood urea and S.
Besides, 40 to 60% of ESRD in Type 2 diabetic patients is not caused by diabetic nephropathy.
These patterns reflect that chances of getting diabetic and non-diabetic renal disease are nearly equal in Type 2 diabetic patients in the absence of diabetic retinopathy. I propose that renal biopsy is indicated in proteinuric Type 2 diabetic patients regardless of presence or absence of diabetic retinopathy for precise diagnosis of DN vs non-diabetic renal disease in such patients.
However, the finding of a negative urinary sediment in patients considered to be at high risk for chronic kidney disease should lead to a repeat examination of the sediment.
Approximately, 20-40% of Type 2 diabetic patients with biopsy proven diabetic nephropathy did not have evidence of diabetic retinopathy. Renal osteodystrophy is relatively rare in diabetic : it takes a long time for the parathyroid glands to become overactive and kidney failure develops relatively quickly in diabetics.
Early diagnosis of NDRD is crucial as appropriate therapy could prolong renal survival in this patient population.
Table 62 provides a brief guide to the interpretation of proteinuria and abnormalities in urine sediment. He developed pulmonary tuberculosis and was started on 4 drugs ATT (RHEZ) on 25th January 2010. However, it may be necessary occasionally to treat kidney bone disease with calcium or vitamin D. It is important to mention that 40% to 60% of ESRD in diabetic patients is associated with non-diabetic primary renal diseases. Percutaneous renal biopsy was done in view of nephrotic proteinuria with well preserved renal function in a diabetic patient. Their diagnosis is important because progressive loss of renal function is faster in diabetic renal disease (diabetic nephropathy) in comparison to Non-Diabetic Nephropathy (NDN). Therefore, presence or absence of diabetic retinopathy did not prove to be significant enough in distinguishing diabetic glomerulosclerosis and NDN in Type 2 diabetic patients.
An even earlier start may be justified in individual case if fluid overload and blood pressure are very difficult to control. Diabetic retinopathy in proteinuric Type 2 diabetic patients may favour diabetic nephropathy but does not exclude non-diabetic renal diseases.
Glomeruli showed feature consistent with diagnosis of focal segmental glomerulosclerosis with chronic tubulointerstitial nephritis. Severe anorexia and persistent vomiting due to kidney failure or delayed emptying of stomach (gastroparesis) is another indication for early dialysis. The renal biopsy is necessary for precise diagnosis of diabetic and non-diabetic renal lesions in proteinuric Type 2 diabetic patients even in the presence of diabetic retinopathy.
It is important to make an individual decision as to when to begin dialysis based on the patient as a whole and not to rely simply on level of kidney function.
A dialysis patient with systemic calciphylaxis exhibiting rapidly progressive visceral ischemia and acral gangrene. Fulminant pulmonary calciphylaxis and metastatic calcification causing acute respiratory failure in a uremic patient. Calciphylaxis associated with cholangiocarcinoma treated with low-molecular-weight heparin and vitamin K. He is still continuing with oral hypoglycemic drug and antihypertensive medication with good control of diabetes and blood pressure.
Acute respiratory failure due to a€?pulmonary calciphylaxisa€? in a maintenance haemodialysis patient.

Statistics on nursing medication errors
Structured education for type 2 diabetes symptoms



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