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Diabetic Nephropathy Osmosis

Diabetic Nephropathy

Diabetic Nephropathy

Maintenance of glycosylated Hb (HbA1c) 7.0 Aggressive BP control, beginning with angiotensin inhibition Primary treatment is strict glucose control to maintain HbA1c 7.0; maintenance of euglycemia reduces microalbuminuria but may not retard disease progression once DN is well established. Glucose control must also be accompanied by strict control of BP to < 130/80 mm Hg, although some experts now recommend BP < 140/90 mm Hg. Some suggest BP should be 110 to 120/65 to 80 mm Hg, particularly in patients with protein excretion of > 1 g/day; however, others claim that BP values < 120/85 mm Hg are associated with increased cardiovascular mortality and heart failure. Angiotensin inhibition is first-line therapy. Thus, ACE inhibitors or angiotensin II receptor blockers are the antihypertensives of choice; they reduce BP and proteinuria and slow the progression of DN. ACE inhibitors are usually less expensive, but angiotensin II receptor blockers can be used instead if ACE inhibitors cause persistent cough. Treatment should be started when microalbuminuria is detected regardless of whether hypertension is present; some experts recommend drugs be used even before signs of renal disease appear. Diuretics are required by most patients in addition to angiotensin inhibition to reach target BP levels. Dose should be decreased if symptoms of orthostatic hypotension develop or serum creatinine increases by more than 30%. Nondihydropyridine calcium channel blockers (diltiazem and verapamil) are also antiproteinuric and renoprotective and can be used if proteinuria does not meaningfully decrease when target BP is reached or as alternatives for patients with hyperkalemia or other contraindications to ACE inhibitors or angiotensin II receptor blockers. In contrast, dihydropyridine calcium Continue reading >>

Diabetes Mellitus (dm)

Diabetes Mellitus (dm)

By Erika F. Brutsaert, MD, Assistant Professor, Albert Einstein College of Medicine; Attending Physician, Montefiore Medical Center Diabetes Mellitus and Disorders of Carbohydrate Metabolism Diabetes mellitus (DM) is impaired insulin secretion and variable degrees of peripheral insulin resistance leading to hyperglycemia. Early symptoms are related to hyperglycemia and include polydipsia, polyphagia, polyuria, and blurred vision. Later complications include vascular disease, peripheral neuropathy, nephropathy, and predisposition to infection. Diagnosis is by measuring plasma glucose. Treatment is diet, exercise, and drugs that reduce glucose levels, including insulin and oral antihyperglycemic drugs. Complications can be delayed or prevented with adequate glycemic control; heart disease remains the leading cause of mortality in DM. There are 2 main categories of diabetes mellitustype 1 and type 2, which can be distinguished by a combination of features (see Table: General Characteristics of Types 1 and 2 Diabetes Mellitus ). Terms that describe the age of onset (juvenile or adult) or type of treatment ( insulin- or non insulin-dependent) are no longer accurate because of overlap in age groups and treatments between disease types. Impaired glucose regulation (impaired glucose tolerance, or impaired fasting glucosesee Table: Diagnostic Criteria for Diabetes Mellitus and Impaired Glucose Regulation* ) is an intermediate, possibly transitional, state between normal glucose metabolism and diabetes mellitus that becomes more common with aging. It is a significant risk factor for DM and may be present for many years before onset of DM. It is associated with an increased risk of cardiovascular disease, but typical diabetic microvascular complications are not very common (album Continue reading >>

Diabetes Mellitus And Polyuria

Diabetes Mellitus And Polyuria

Diabetes comes from the Greek word which means “siphon”. There are two distinct disorders that share the first name diabetes: diabetes mellitus and diabetes insipidus. This is because both disorders cause polyuria, or excessive urine output. Diabetes insipidus is a disorder of urine concentration which we will discuss in spring quarter. Diabetes mellitus is a disorder of blood glucose regulation, which results from a deficiency in the action of the hormone insulin. This may be due to autoimmune destruction of the insulin-secreting cells of the pancreas (type 1 diabetes mellitus) or it may result from a problem in the responsiveness of tissues to insulin, known as insulin resitance (type 2 diabetes mellitus). With either disorder, the result is hyperglycemia, or high levels of glucose in the plasma. How does hyperglycemia cause excessive urine production? To answer this, we need to understand a little bit about how the kidney works. Each kidney contains about a million functional units called nephrons (blue structure in the figure). The first step in the production of urine is a process called filtration (green arrow). In filtration, there is bulk flow of water and small molecules from the plasma into Bowman’s capsule (the first part of the nephron). Because of the nonspecific nature of filtration, useful small molecules such as glucose, amino acids, and certain ions end up in the forming urine, which flows into the kidney tubules. To prevent the loss of these useful substances from the body, the cells lining the kidney tubules use epithelial transport to transfer these substances out of the forming urine and back into the extracellular fluid. This process is known as reabsorption (purple arrows). Under normal circumstances, 100% of the glucose that is filtered is Continue reading >>

File:diabetic Nephropathy.webm

File:diabetic Nephropathy.webm

English: What is Diabetic Nephropathy? Diabetic Nephropathy is the kidney damage that results from both type I and type II diabetes. Sources: First Aid 2017 Pathoma Robbins & Cotran Pathologic Basis of Disease 9e Step Up to Medicine 4th Edition 2016 Woredekal Y, Friedman EA. Chapter 54. Diabetic Nephropathy. In: Lerma EV, Berns JS, Nissenson AR. eds. CURRENT Diagnosis & Treatment: Nephrology & Hypertension New York, NY: McGraw-Hill; 2009. . Accessed March 10, 2017. open.osmosis.org (Displayed at end of video) This file is licensed under the Creative Commons Attribution-Share Alike 4.0 International license. to share to copy, distribute and transmit the work attribution You must attribute the work in the manner specified by the author or licensor (but not in any way that suggests that they endorse you or your use of the work). share alike If you alter, transform, or build upon this work, you may distribute the resulting work only under the same or similar license to this one. CC BY-SA 4.0 Creative Commons Attribution-Share Alike 4.0 truetrue Continue reading >>

Diabetic Neuropathy (diabetes Nerve Damage)

Diabetic Neuropathy (diabetes Nerve Damage)

Home Current Health Articles Diabetic Neuropathy (Diabetes Nerve Damage) Diabetic Neuropathy (Diabetes Nerve Damage) Diabetic neuropathy is the nerve dysfunction and damage that is a result of long-standing and often poorly controlled diabetes mellitus ( sugar diabetes ). It is the most common complication of diabetes mellitus and these neurological disturbances may affect more than half of all cases of long term diabetes. Diabetic neuropathy is a broad therm that encompasses a variety of clinical neurological syndromes. It can be in the form of focal neuropathy, polyneuropathy, or autonomic neuropathy. Although neuropathy is a common complication of long standing and uncontrolled diabetes mellitus, it is often ignored until the late stages of the disease. At this point, symptoms like paresthesia, numbness or tingling, especially of the legs, affects daily functioning and leads to repeated injuries that predisposes to the formation of diabetic ulcers. The exact mechanism behind diabetic neuropathy in not fully understood but it is generally accepted to be due to many factors. There are many other types of neuropathy but in this case it is attributed to diabetes mellitus if the condition is present in a diabetic patient and no other causes of neuropathy is evident. Diabetes can produce acute and often self-limiting type of neuropathies that is likely to result from vascular effects of diabetes. This means that the nerve damage arises as a result of compromised blood flow through the blood vessels of nerves. The more common, chronic type of neuropathies in diabetes often results from metabolic factors related to diabetes. The most prominent factor linked to the development of diabetic neuropathy is long standing hyperglycemia (high blood glucose levels). With long standi Continue reading >>

Beware: Diabetes Results In Significant Electrolyte Disturbances

Beware: Diabetes Results In Significant Electrolyte Disturbances

Incidence of type 2 diabetes is increasing rapidly. It accounts for up to half of all cases of new-onset diabetes in young people. Dysfunction in glucose homeostasis impacts acid-base regulation. In addition, injury to organs as a result of diabetes and antidiabetic drugs contribute to this dysregulation. Hyponatremia is associated with increased plasma glucose concentrations. Higher glucose concentration results in an osmotic force that draws water to the extracellular space. This dilutes extracellular sodium and leads to lower plasma sodium levels. This is why measured sodium levels need to be altered with a correctional factor during hyperglycemic crises. Sodium levels can fluctuate wildly during treatment of hyperglycemic crises due to osmotic diuresis and fluid intake, as well. Many medications commonly used in the management of diabetes result in hyponatremia as well. Tricyclic antidepressants, used in the treatment of diabetic neuropathy, stimulate vasopressin and lead to lower levels. First-generation sulfonylureas and insulin are also known to cause hyponatremia by augmenting the effects of vasopressin at the renal collecting ducts. Potassium levels are also altered in diabetes. High plasma glucose concentrations lead to potassium efflux to the extracellular space, causing hyperkalemia. Diabetic ketoacidosis is a clinically significant acid-base disturbance in diabetes. It occurs due to an increase in the rate of hepatic ketoacid generation. Bicarbonate degrades to carbon dioxide and water, and anion-gap acidosis results. It is typically treated with insulin and volume resuscitation. Alkali therapy is not typically appropriate; bicarbonate will regenerate upon administration of insulin and the oxidation of ketoanions. Rarely, metformin can lead to acidosis. The Continue reading >>

Monitoring And Complications Of Diabetes

Monitoring And Complications Of Diabetes

These will depend on the treatment. Type 2 diabetes treated by diet and oral agents can get away with measuring their levels once or twice a week. These patients should check their fasting glucose levels. Patients on insulin need to monitor much more carefully, in order to adjust the dose of insulin. There are two types of insulin – short acting and long acting. Long acting insulin has be monitored typically 12 hours after it was administrated, whilst short acting insulin should be monitored 90 to 120 minutes after administration. Patients should check their glucose levels regularly. This could consist of checking twice every day, or it ay be that they check 4 times a day, but only on a couple of days each week. As a doctor, it is also important to check the patients monitoring technique, and make sure they have an action plan for what to do if they get readings outside of the normal level. HbA1c is glycosylated haemoglobin. It is formed when haemoglobin comes into contact with glucose, and is formed via a non-enzymatic pathway. When glycosylation occurs via a non-enzymatic pathway, we call it glycation. This process occurs all the time, but the rate of the reaction is proportional to the concentration of glucose. During its 120 day lifecycle, a red blood cell comes into contact with glucose. Some of this glucose will become joined to haemoglobin within the red cell through glycation. In individuals with poorly controlled glucose, the haemoglobin is more likely to come into contact with a glucose molecule, and thus more HbA1c is formed! Fructosamide can be used in similar tests – in this case fructose reacts with albumin to produce fructosamide. This is generally used in situations where HbA1c cannot be tested, such as: Glycation is the process by which a protein or Continue reading >>

Hyponatremia In Diabetes Mellitus: Clues To Diagnosis And Treatment

Hyponatremia In Diabetes Mellitus: Clues To Diagnosis And Treatment

Department of Internal Medicine, School of Medicine, University of Ioannina, Ioannina, Greece Citation: Liamis G, Tsimihodimos V, Elisaf M (2015) Hyponatremia in Diabetes Mellitus: Clues to Diagnosis and Treatment. J Diabetes Metab 6: 560. doi: 10.4172/2155-6156.1000560 Copyright: © 2015 Liamis G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Hyponatremia is the most common electrolyte abnormality in clinical practice and is associated with increased morbidity and mortality [1,2]. Even small decreases of serum sodium are associated with increased probability for adverse outcomes (cognitive impairment, falls, osteoporosis and fractures) [3]. Decreased serum sodium levels are occasionally observed in patients with diabetes mellitus and can be attributed to numerous underlying pathogenetic mechanisms (Table 1) [4,5]. A) Non hypotonic hyponatremia With increased Posm: Hyperglycemia - induced (dilutional) With normal Posm: Pseudohyponatremia (marked hypertriglyceridemia and hyperproteinemia) B) Hypotonic hyponatremia • Hypovolemia-induced • Drug –induced hyponatremia (mainly with thiazides and first generation sulphonylureas) • Diabetes mellitus - associated hyponatremia • Syndrome of inappropriate antidiuresis associated with coexisting disorders or administered drugs • Chronic renal failure (diabetic nephropathy) or associated with the syndrome of hyporeninemichypoaldosteronism Table 1: Causes of hyponatremia in diabetic patients. The direct measurement of serum osmolality (Posm) can differentiate be Continue reading >>

Diabetes Mellitus

Diabetes Mellitus

4 Treatment The clinical syndrome described by the term diabetes mellitus results from intolerance to glucose. It is a chronic disease caused by an absolute or relative deficiency of insulin and, although all body systems are ultimately affected, it is primarily a disorder of carbohydrate metabolism. The approximate incidence of the disease is 13 cases/10,000 dogs years at risk[1]. Insulin is produced in the beta cells of the pancreatic islets of Langerhans and is released into the circulation to act on specific cell-surface receptors. Its release is stimulated by rising blood glucose concentration and it is principally insulin which is responsible for the post-prandial cellular glucose uptake and storage observed in humans and dogs. Several hormones (including corticosteroids, progesterone, oestrogen, growth hormone, glucagon and catecholamines) have an antagonistic effect to insulin and cause the blood glucose concentration to increase. Interruptions at any stage in this pathway may produce the clinical syndrome of diabetes mellitus, including: Failure to produce insulin resulting in an absolute deficiency - This may be due to degenerative changes in the beta cells or it may occur with severe exocrine pancreatic disease that disrupts the islets of Langerhans. The major example of the latter disease process is pancreatitis and, in cases of this diesase, diabetes mellitus is often found concurrently with exocrine pancreatic insufficiency. Degeneration of the beta cells, whether it involves the immune system or not, results in type 1 diabetes mellitus and miniature Poodles, Dachshunds and terriers appear to be predisposed to this condition. In humans, it is speculated that immune responses directed at certain pathogens (notably coxsackie virus B1) may cross-react with an Continue reading >>

Diabetic Kidney Disease: The Animated Explanation

Diabetic Kidney Disease: The Animated Explanation

Diabetic Kidney Disease: The Animated Explanation People with diabetes are smarter than average when it comes to knowing their bodies and the inner workings of cells, blood vessels, and the ever-frustrating pancreas. So if youre reading this, you may be smarter than the average bear when it comes to kidney knowledge. Up to 40 percent of people with diabetes will develop kidney disease, or nephropathy, and it affects those with all types of diabetes as its a complication of high blood sugar. Diabetes is the leading cause of kidney failure in developed countries. The kidneys are responsible for filtering our blood and sending out waste products in the urine. Each kidney has millions of nephrons, which are the kidneys basic functional unit. These nephrons receive blood through a capillary bed called a glomerulus. Blood moves through the glomerulus into the nephrons for filtration, and large cells and proteins are kept out of the glomerulus by the glomerulus membrane. Chronic high blood sugar damages this process by: Thickening the the blood vessel that takes blood out of the glomerulus, causing decreased outflow and increased pressure within the glomerulus. Increased blood flow into the glomerulus because of the backup in outflow. Thickening of the glomerulus membrane, allowing albumin proteins into the glomerulus (it sounds counterintuitive, but a thicker membrane means less compact filtration). This causes hyperfiltration, and more albumin proteins slip into the kidneys and into the urine, causing albuminuria, which is the first stage of kidney disease. Eventually the kidney starts to burn out, leading to decreased filtration, and finally to renal failure, or kidney failure. This stage requires a kidney transplant or dialysis . In the early stages of kidney disease ther Continue reading >>

Diabetic Nephropathy

Diabetic Nephropathy

Author: Vecihi Batuman, MD, FASN; Chief Editor: Romesh Khardori, MD, PhD, FACP more... Diabetic nephropathy is a clinical syndrome characterized by the following [ 1 ] : Persistent albuminuria (>300 mg/d or >200 g/min) that is confirmed on at least 2 occasions 3-6 months apart Progressive decline in the glomerular filtration rate (GFR) Elevated arterial blood pressure (see Workup) Proteinuria was first recognized in diabetes mellitus in the late 18th century. In the 1930s, Kimmelstiel and Wilson described the classic lesions of nodular glomerulosclerosis in diabetes associated with proteinuria and hypertension. (See Pathophysiology.) By the 1950s, kidney disease was clearly recognized as a common complication of diabetes, with as many as 50% of patients with diabetes of more than 20 years having this complication. (See Epidemiology.) Currently, diabetic nephropathy is the leading cause of chronic kidney disease in the United States and other Western societies. It is also one of the most significant long-term complications in terms of morbidity and mortality for individual patients with diabetes. Diabetes is responsible for 30-40% of all end-stage renal disease (ESRD) cases in the United States. (See Prognosis.) Generally, diabetic nephropathy is considered after a routine urinalysis and screening for microalbuminuria in the setting of diabetes. Patients may have physical findings associated with long-standing diabetes mellitus. (See Clinical Presentation.) Good evidence suggests that early treatment delays or prevents the onset of diabetic nephropathy or diabetic kidney disease. This has consistently been shown in both type1 and type 2 diabetes mellitus. (See Treatment and Management). Regular outpatient follow-up is key in managing diabetic nephropathy successfully. ( Continue reading >>

Osmotic Nephrosis - An Overview | Sciencedirect Topics

Osmotic Nephrosis - An Overview | Sciencedirect Topics

Kanwar Nasir M. Khan1, ... Carl L. Alden3, in Haschek and Rousseaux's Handbook of Toxicologic Pathology (Third Edition) , 2013 Osmotic nephrosis refers to a non-specific histopathologic finding rather than defining a specific entity characterized by vacuolization and swelling of the renal proximal tubular cells. Glucose and sucrose are reabsorbed by pinocytosis, leading to vacuolization of PCTs representing hydropic swelling of the phagolysosome (Figure 47.25). Post-prandial phagolysosomal vacuoles occur normally in all species. Mannitol, hydroxyethyl starch, dextran, and contrast media induce the same change. The functional impact of this change is minimal, and the vacuolization actually may be a transient adaptive response. Acute kidney injury and chronic kidney failure have been reported in rare cases for example, after surgical placement of an anti-adhesive barrier of macromolecular polysaccharides in the peritoneal cavity. Lifetime rodent studies of mannitol have not revealed toxic or tumorigenic consequence of the osmotic change. Heather K. Lehman, Mark Ballow, in Pediatric Allergy: Principles and Practice (Third Edition) , 2016 Acute renal failure is a rare but significant complication of IVIG treatment. Histopathologic findings of acute tubular necrosis, vacuolar degeneration and osmotic nephrosis are suggestive of osmotic injury to the proximal renal tubules. Fifty-five percent of the cases were in patients treated for idiopathic thrombocytopenic purpura (ITP), and less than 5% involved patients with primary immunodeficiency.55 This complication may relate to the higher doses of IVIG used in ITP. The majority of the cases were treated successfully with conservative treatment, but deaths were reported in 17 patients who had serious underlying conditions. Report Continue reading >>

Nephrogenic Diabetes Insipidus

Nephrogenic Diabetes Insipidus

Not to be confused with Neurogenic diabetes insipidus. Nephrogenic diabetes insipidus (also known as renal diabetes insipidus) is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central/neurogenic diabetes insipidus, which is caused by insufficient levels of antidiuretic hormone (ADH, that is, arginine vasopressin or AVP). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to ADH, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water. Signs and symptoms[edit] The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with excessive thirst and excretion of a large amount of dilute urine. Dehydration is common, and incontinence can occur secondary to chronic bladder distension.[1] On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, ADH levels are likely to be abnormal or raised. Polyuria will continue as long as the patient is able to drink. If the patient is unable to drink and is still unable to concentrate the urine, then hypernatremia will ensue with its neurologic symptoms.[citation needed] Causes[edit] Acquired[edit] Nephrogenic DI (NDI) is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including amyloidosis,[2] polycystic kidney disease,[3] electrolyte imbalance,[4][5] or some other kidney defect.[2] The major causes of acquired NDI that produce clinical symptoms (e.g. polyuria) in the adult are lithium toxicity and high blood calcium. Chronic lithium ingestion – appears to affect the tubules by enterin Continue reading >>

Osmotic Polyuria: An Overlooked Mechanism In Diabetic Nephropathy

Osmotic Polyuria: An Overlooked Mechanism In Diabetic Nephropathy

Diabetic nephropathy is a common and severe complication that occurs in ∼40% of patients with a long-standing type II diabetes mellitus and in a lesser proportion of subjects with type I diabetes. It occurs usually concomitantly with other microvascular complications of diabetes such as diabetic retinopathy and/or neuropathy that let some scholars view diabetic nephropathy as one of several clinical syndromes resulting from diabetic injury to microvessels. Abnormal microalbuminuria has emerged as a clinical risk factor for renal failure in diabetic renal disease as well as for cardio-vascular disease in general and specifically in diabetes. These epidemiological observations together with the experimental recognition that glomerular visceral epithelial cells (podocytes) are an early target in diabetic renal injury have given rise to the view that diabetic nephropathy may, in fact, be initially and primarily a glomerular disease and tubulo-interstitial nephropathy may be secondary to glomerular proteinuria and/or ischaemia given that peritubular capillaries are located downstream of efferent arterioles. Clinical–pathological correlations have drawn attention that renal failure in diabetic nephropathy is more closely determined by tubulo-interstitial injury and fibrosis than by diabetic nodular and/or diffuse glomerular sclerosis [1,26]. Findings from experimental in vitro studies and in vivo observations in animal models have derived a series of hypotheses as to the mechanisms of tubulo-interstitial injury. Most of these invoke high glucose levels and the increased proportion of glycation of structural and regulatory cell proteins and extracellular proteins (such as glycated albumin and modified ultrafiltered proteins) at the initiation of an injury cascade. Response Continue reading >>

Peripheral Neuropathy Treatment

Peripheral Neuropathy Treatment

4. HOW MIGHT ONE CONSIDER TREATING THIS CONDITION? 5. WHAT ARE THE CONVENTIONAL MEDICAL TREATMENTS? DO THEY EVEN WORK? Pain is temporary. It may last a minute, or an hour, or a day, or a year, but eventually it will subside and something else will take its place. If I quit, however, it lasts forever. That surrender, even the smallest act of giving up, stays with me. So when I feel like quitting, I ask myself, which would I rather live with? I think this perspective, above, is interesting because it allows one to cope when feeling pain but when it comes to chronic peripheral neuropathy that I see most commonly he is dead wrong. I dont think there is anything that slowly destroys a human being more than chronic pain. I see quite a bit of chronic pain in my daily job and decided to write a quick blog about it because of the shear number of emails I have received to speak on this topic. Neuropathy is a malfunctioning of a nerve or a group of nerves. It can be caused by many factors. Some of them are nutritional deficiency, drug toxicity, trauma, vascular damage, poisoning or disease states like diabetes. The one basic premise that is common to all causes is that there is a disruption of normal nerve impulse transmission from the damaged nerve and that information is sent to the central nervous system in the brain and spinal cord for further processing. This malformed messaged could in fact be perceived by the brain as a sensation associated with pain, numbness, or the muscle innervated by this nerve to be non functional. The most common cause in the USA is diabetic neuropathy. The second most common cause is trauma. This could be physical or iatrogenic. Neuropathy is generally associated with three sensations. 1. Paraesthesia- which is numbness or tingling 3. Dyesthesia- w Continue reading >>

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