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People with diabetes often use a blood sugar monitoring device to help them test and control sugar levels. Diabetes is a condition characterized by high blood sugar (glucose) levels, and Type 2 diabetes is the most common form. Type 2 diabetes is a chronic disease, and left untreated, it can cause serious health complications.
Exactly why the body fails to respond to insulin, a phenomenon called insulin resistance, is not known, but risk factors include being overweight, inactive or older than 45. In contrast to Type 2 diabetes, Type 1 diabetes occurs when the pancreas makes little or no insulin.
According to the National Institutes of Health, early symptoms of Type 2 diabetes include increased thirst, increased urination, hunger, fatigue and more frequent or slow to heal infections, such as bladder, kidney and skin infections. After many years, Type 2 diabetes can lead to serious health issues, including eye problems and blindness, nerve damage that causes pain, tingling and numbness, kidney damage and poor blood flow to the legs and feet, the NIH says.
Some people learn they have diabetes through routine blood testing, such as when a doctor checks blood glucose levels during an annual exam, or for diabetes screening, Sood said.
Normal blood sugar varies from person to person, but a normal range for fasting blood sugar (the amount of glucose in your blood six to eight hours after a meal) is between 70 and 100 milligrams per deciliter.
People who have a family history of Type 2 diabetes should talk to their doctor about being screened for the condition, Sood said, because a family history of the disease increases the risk of developing Type 2 diabetes.
It is important for people with Type 2 diabetes to manage their weight and have a well-balanced diet. Physical activity is also important, and those with Type 2 diabetes should aim to exercise for at least 30 minutes at day.
Weight loss surgery, or bariatric surgery, is also an option for very obese patients who have trouble managing their diabetes with diet, exercise and medications, the NIH says. Sood said she recommends people who are diagnosed with Type 2 diabetes lose at least five to 10 percent of their current body weight. Type 2 diabetes has traditionally been seen as a progressive disease that is managed rather than cured.
But recent studies have suggested that in some cases, Type 2 diabetes can be reversed with weight loss surgery, or by following an extreme diet that mimics surgery.
Another study, published in 2011 in the journal Diabetologia, found that people with Type 2 diabetes who followed an extreme diet of extreme diet of just 600 calories a day saw their blood glucose levels return to normal in about a week, and most were still diabetes-free three months after they stopped the diet. A 2012 study from the Centers for Disease Control and Prevention found that some people may be able to return their blood sugar levels to normal by following a diet and exercise program, although this is very rare. Diabetic neuropathy (DN) is a descriptive term meaning a demonstrable disorder, either clinically evident or sub-clinical, that occurs in the setting of diabetes mellitus without other causes for peripheral neuropathy. In this review, we have summarized the epidemiology, clinical features, pathogenesis, classification and diagnosis of diabetic neuropathy. The true prevalence is not known and depends on the criteria and methods used to define neuropathy.
The acute onset symmetric neuropathies include diabetic neuropathic cachexia which is an uncommon painful sensory neuropathy occurring in type 1 diabetes in the setting of poor glucose control and weight loss. The asymmetric neuropathies can also be divided into those with acute onset and those with gradual onset. An easy and practical way to approach this conundrum of classifications is to classify diabetic neuropathy as typical and atypical. Diabetic neuropathy has a wide spectrum of clinical manifestations, the most common being distal symmetrical sensorimotor loss in the classical 'stocking-glove' distribution (DSPN). Diabetic sensorimotor polyneuropathy (DSPN) is a mixed neuropathy with small and large fibre sensory, motor and autonomic involvement in various combinations.
Diabetic small fibre neuropathy (DSFN): Small fibre predominant neuropathy in diabetes is being increasingly recognised and is an early manifestation of peripheral nerve involvement.
Diabetic autonomic neuropathy affects various organs of the body resulting in cardiovascular, gastrointestinal, urinary, sweating, pupils, and metabolic disturbances. Diabetic lumbar radiculoplexopathy: Also known as Diabetic amyotrophy or proximal diabetic neuropathy, it presents with abrupt onset, often unilateral severe pain in the anterior thigh, buttock or lower back followed by weakness and wasting in the thigh. Diabetic truncal radiculoneuropathy: It presents with abrupt onset severe pain (burning, stabbing or belt like) with contact hyperesthesia in the thoracic spine, flank, rib cage or upper abdomen.
Cranial neuropathy: The oculomotor nerves are most often affected (third, sixth, rarely fourth). Patients with diabetes can also present with mononeuritis multiplex without an underlying rheumatological cause and are at increased risk of entrapment mononeuropathy.
Chronic hyperglycaemia is an important contributing factor leading to diabetic complications.
It is generally agreed that diabetic neuropathy should not be diagnosed on the basis of one symptom, sign, or test alone. Traditionally, nerve conduction studies (NCSs) have been the most frequently used diagnostic tool for DSPN.
Pathologically, DSFN is characterized by degeneration of distal terminations of small-diameter sensory fibres, observed as low IENF density (IENFD) on histological analysis of tissue from patients with the condition. Over the past decade, the non-invasive technique of in vivo confocal microscopy of the cornea has been developed, mainly for use in patients with diabetic neuropathy. Microneurography has made recording of single Ad-fibre and C fibre activity possible, and provides a direct method for measuring sympathetic activity. To conclude, diabetes is associated with a variety of chronic and acute neuropathies, the commonest form being distal symmetric polyneuropathy.
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Funding is constantly needed for new projects and to update and refurbish existing facilities. Our in house labs will give you immediate results of your Hemoblobin a1c and our in house pharmacy stocks all of your diabetes medications. Diseases of the kidney are a common finding in people with diabetes, with up to half demonstrating signs of kidney damage in their lifetime (1–3).
The classic description of diabetic nephropathy is of a progressive increase in proteinuria in people with longstanding diabetes followed by declining function that eventually can lead to end stage renal disease (ESRD) ( Figure 2 ) (1,9,10).
The earliest stage of diabetic nephropathy is hyperfiltration, where the glomerular filtration rate (GFR) is significantly higher than normal. It is important to note that the rate of progression can vary between individuals, and that the clinical markers of the disease (i.e. People with diabetes (particularly type 2 diabetes) often develop kidney diseases other than diabetic nephropathy. Screening for kidney disease in people with diabetes involves an assessment of urinary albumin excretion and a measurement of the overall level of kidney function through an estimation of the GFR.
When screening for albuminuria, the test of choice is the random urine albumin-to-creatinine ratio (urinary ACR). The serum creatinine is the most common measurement of kidney function; however, it can inaccurately reflect renal function in many scenarios, particularly in extremes of patient age or size (33,34). The eGFR is useful for assessing chronic changes in renal function but should not be used in situations where kidney function is changing rapidly. Urinalysis findings of red blood cell casts are not a common finding in renal disease due to diabetes, and white blood cell casts or heme-granular casts are not compatible with a diagnosis of kidney disease due to diabetes. Although 24-hour collections are not needed for routine screening in diabetes, they can be useful when there is doubt about the accuracy of an eGFR, when screening for nonalbumin urinary proteins (e.g. People with diabetes should undergo annual screening for the presence of kidney disease when they are clinically stable and not suspected of having acute kidney injury or nondiabetic renal disease. Screening for CKD in people with diabetes should be performed with a random urine ACR and a serum creatinine that is then converted into an eGFR (Figure 3 ).
Once a diagnosis of CKD has been made, a urine sample for dipstick and microscopy should be ordered.
Optimal glycemic control established as soon as possible after diagnosis will reduce the risk of development of diabetic nephropathy (38–42).
All people with CKD are at risk for cardiovascular (CV) events and should be treated to reduce these risks (see Vascular Protection chapter, p. The progression of renal damage in diabetes can be slowed through intensive glycemic control (38) and optimization of BP (55). In CKD from causes other than diabetic nephropathy, ACE inhibition has been shown to reduce proteinuria, slow progressive loss of glomerular filtration rate and delay the need for dialysis (70,71). A variety of strategies to more aggressively block the RAAS have been studied in kidney disease, including combining RAAS blockers or using very high doses of a single RAAS blocker.
Several classes of medications used commonly in people with diabetes can reduce kidney function during periods of intercurrent illness and should be discontinued when patients are unwell, in particular when they develop significant intravascular volume contraction due to reduced oral intake or excessive losses due to vomiting or diarrhea.


Drugs that block the RAAS reduce intraglomerular pressure, which, in turn, leads to a rise in serum creatinine of up to 30%, which then stabilizes (79). Mild-to-moderate hyperkalemia can be managed through dietary counselling, Diuretics, in particular furosemide, can increase urinary potassium excretion. As the use of RAAS blockers during pregnancy has been associated with congenital malformations, women with diabetes of childbearing age should avoid pregnancy if drugs from these classes are required (84). Many medications need to have their dose adjusted in the presence of low kidney function, and some are contraindicated in people with significant disease. Most people with CKD and diabetes will not require referral to a specialist in renal disease. Shading shows how adjusted relative risk is ranked for 5 outcomes from a meta-analysis of general population cohorts: all-cause mortality, cardiovascular mortality, kidney failure treated by dialysis and transplantation, acute kidney injury, and progression of kidney disease.
39 Anonymous Effect of intensive therapy on the development and progression of diabetic nephropathy in the Diabetes Control and Complications Trial. 40 Anonymous Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). 41 Retinopathy and nephropathy in patients with type 1 diabetes four years after a trial of intensive therapy. 43 Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38.
More than 29 million Americans have diabetes (the majority of which are Type 2), but 8 million don't know they have it, according to a 2014 report from the Centers for Disease Control and Prevention.
When the body's cells fail to respond properly to insulin, sugar builds up in the bloodstream, eventually leading to Type 2 diabetes. This is mostly done through the kidneys, and the body also gets rid of water along with the sugar, Sood said.
People with Type 2 diabetes should consult with their doctor about how often they should check their blood sugar levels, which is done with a device called a glucose meter, according to the NIH. While some people can control Type 2 diabetes with diet and exercise alone, others may need to take medications, such as metformin, according to Mayo. Just because a patient can stop taking diabetes medications does not mean their diabetes is cured, the NIH says. A 2011 study in the journal Science Translational Medicine said that about 50 to 80 percent of patients who have gastric bypass surgery (a type of weight-loss surgery) see a reduction in their blood glucose levels that's enough for them to be considered free of Type 2 diabetes.
However, the study was small, with just 11 people, and experts say that such an extreme diet would be hard to keep up, and it's not clear how long diabetes will remain in remission after the diet is stopped. In the study, which involved 4,500 people with Type 2 diabetes, 1.3 percent were able to achieve normal blood sugar levels with diet and exercise. She has a masters degree in journalism from New York University's Science, Health and Environmental Reporting Program. Of patients attending a diabetes clinic, 25% volunteered symptoms, but 50% were found to have neuropathy after a simple clinical test such as eliciting the ankle reflex or vibration perception test. Insulin neuritis, which is again a painful neuropathy is seen with initiation of insulin treatment. Diabetic truncal radiculoneuropathy, radiculoplexopathy or diabetic amyotrophy, cranial neuropathies (third or sixth nerves) and mononeuritis multiplex constitute the acute onset group. It presents with pain and dyesthesias in the feet and is difficult to diagnose, as the clinical examination and nerve conduction studies may be normal. Orthostatic hypotension, resting tachycardia, and heart rate unresponsiveness to respiration are a hallmark of diabetic autonomic neuropathy. Diabetic third nerve palsy presents with abrupt onset retro-orbital pain, followed by double vision, unilateral ptosis, restriction of medial and upgaze and sparing of the pupil. As with most other axonal neuropathies, the central feature of DSPN is reduced distal lower extremity sensory nerve action potential amplitudes.14 But over the years it has been realised that diagnosis of DSFN (Ad-fibres and C fibres) is challenging as the clinical picture can be difficult to interpret and results from nerve conduction studies are often normal. For the evaluation of small nerve fibre dysfunction, only temperature thresholds are measured. In the nerve axon reflex, C nociceptive fibres are stimulated by acetylcholine iontophoresis producing vasodilatation which can be quantitatively measured and serves as a measure of small fibre function.22 The laser Doppler imaging flare test evaluates 44°C heat-induced vasodilation and is reduced in subjects with IGT and type 2 diabetic patients with and without neuropathy. Performing an annual screening through a good neurological history and clinical examination and using a sensitive screening tool can facilitate an early diagnosis.
Pop-Busui R, Evans GW, Gerstein HC, Fonseca V, Fleg JL, Hoogwerf BJ, et al; Action to Control Cardiovascular Risk in Diabetes Study Group. Progression of diabetic nephropathy can be slowed through the use of medications that disrupt the renin-angiotensin-aldosterone system.
Key risk factors for diabetic nephropathy include long duration of diabetes, poor glycemic control, hypertension, male gender, obesity and cigarette smoking.
Identification of hyperfiltration is not clinically useful, as it is difficult to determine from routine testing.
Kidney biopsy series in type 2 diabetes have found that nondiabetic glomerular disease, particularly hypertensive or ischemic nephropathy, is as common as diabetic nephropathy in people with diabetes (7). Persistent abnormalities of either urinary albumin excretion or GFR, or significant urinalysis abnormalities, lead to the diagnosis of kidney disease in people with diabetes.
Indeed, in people with diabetes, the GFR usually will be less than half of normal before the serum creatinine exceeds the lab normal range (35). For this reason, a variety of methods have been developed to better estimate the level of glomerular filtration by combining the patient's serum creatinine with factors such as age, weight, and gender.
Dehydration and other conditions that lead to intravascular volume contraction can lead to a transient decline in renal function. Although persistent microscopic hematuria can occur in about 20% of people with diabetic nephropathy, its presence should lead to the consideration of other urological or nephrological conditions. Screening should be delayed in the presence of conditions that can cause transient albuminuria ( Table 3 ) or a transient fall in eGFR.
This can be delayed 5 years from the onset of type 1 diabetes but should begin immediately at the time of diagnosis of type 2 diabetes. In the absence of any significant abnormalities other than proteinuria, then a presumptive diagnosis of kidney disease due to diabetes is made.
Optimal BP control also appears to be important in the prevention of diabetic nephropathy, although the results have been less consistent (41,43–45).
Progression of diabetic nephropathy can be slowed through the use of an ACE inhibitor or ARB (56), independent of their effect on BP, and these 2 medication classes appear to be equally effective for cardiorenal protection (57,58).
The issue of whether ARBs and ACE inhibitors are similarly effective in CKD that is not caused by diabetic nephropathy remains controversial (72,73).
These strategies reduce proteinuria but have not been proven to improve patient outcomes in diabetic nephropathy (74–77) and come at a risk of increased acute renal failure, typically when a patient develops intravascular volume contraction (78).
Diuretics can exacerbate intravascular volume contraction during periods of intercurrent illness. Although these drugs can be used safely in patients with renovascular disease, these patients may have an even larger rise in serum creatinine when these drugs are used (80–82).
Sodium bicarbonate (500 to 1300 mg orally twice a day) can also increase urinary potassium excretion, especially amongst individuals with a metabolic acidosis as demonstrated by a low serum bicarbonate level. If a woman with diabetes receiving such medications wishes to become pregnant, consideration should be given to their discontinuation prior to conception. Appendix 6 lists some medications commonly used in people with diabetes and how they should be used if kidney dysfunction is present. However, specialist care may be necessary when renal dysfunction is severe, when there are difficulties implementing renal-protective strategies or when there are problems managing the sequelae of renal disease (85).
In adults, screening for CKD in diabetes should be conducted using a random urine ACR and a serum creatinine converted into an eGFR [Grade D, Consensus]. All patients with diabetes and CKD should receive a comprehensive, multifaceted approach to reduce cardiovascular risk (see Vascular Protection, p. People with diabetes on an ACE inhibitor or an ARB should have their serum creatinine and potassium levels checked at baseline and within 1 to 2 weeks of initiation or titration of therapy and during times of acute illness [Grade D, Consensus]. Combination of agents that block the renin-angiotensin-aldosterone system (ACE inhibitor, ARB, DRI) should not be routinely used in the management of diabetes and CKD [Grade A, Level 1 (89,90) ]. This symptom can sometimes be confusing to patients, because diabetes is associated with obesity and too much weight gain, Sood said.
Keeping track of your glucose levels will let you and your doctor know if changes need to be made to your diet, activity or medications.
She also holds a Bachelor of Science in molecular biology and a Master of Science in biology from the University of California, San Diego. The symptoms start as numbness, tingling, burning or pricking sensation in the feet and spread proximally in a length dependent fashion (stocking glove pattern).
Aneurysm must be excluded by neuroimaging in atypical cases (pupillary involvement or absence of pain).
The other common parameter measured by QST in clinical practice, reflecting large fiber involvement is vibration sensation. More sensitive and quantitative measures of detecting early peripheral nerve injury including skin biopsy for intra-epidermal and dermal nerve fiber density and confocal corneal microscopy, hold promise to identify neuropathy patients early in their disease course.


The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: the Rochester Diabetic Neuropathy Study.
Prevalence of microvascular complications in newly diagnosed patients with type 2 diabetes.
Frequency of cardiac autonomic neuropathy in patients with type 2 diabetes mellitus reporting at a teaching hospital of Sindh. Diabetic neuropathies: update on definitions, diagnostic criteria, estimation of severity, and treatments. Corneal confocal microscopy: a non-invasive surrogate of nerve fibre damage and repair in diabetic patients. On the relationship between nociceptive evoked potentials and intraepidermal nerve fiber density in painful sensory polyneuropathies. The LDI flare: a novel test of C-fiber function demonstrates early neuropathy in type 2 diabetes.
Clinical examination versus neurophysiological examination in the diagnosis of diabetic polyneuropathy. A practical two-step quantitative clinical and electrophysiological assessment for the diagnosis and staging of diabetic neuropathy. Effects of cardiac autonomic dysfunction on mortality risk in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial.
Kidney disease can be a particularly devastating complication, as it is associated with significant reductions in both length and quality of life (5,6). Persistent albuminuria is considered the earliest clinical sign of diabetic nephropathy ( Table 1 ). Additionally, aggressive control of blood pressure (BP) and glycemia, and the use of renal protective drugs can slow or stop progression of diabetic nephropathy.
People with type 1 diabetes are not expected to have kidney disease at the time of onset of diabetes, so screening can be delayed until the duration of diabetes exceeds 5 years. The random urine for albumin is insufficient, as the urinary albumin concentration can vary due to urine concentration (24).
When such conditions are present, screening for kidney disease should be delayed to avoid false positives. When such conditions are present, assessment of the level of kidney function may be clinically necessary but should not be used to assess the stage of CKD. Table 2 lists other clinical clues that may point to a renal diagnosis other than kidney disease due to diabetes.
An abnormal screening test should be confirmed by repeat testing of the eGFR within 3 months, and 2 more random urine ACRs ordered during that interval. The presence of clinical or laboratory abnormalities suggesting nondiabetic kidney disease indicates the need for appropriate workup or referral.
Blockade of the renin-angiotensin-aldosterone system (RAAS) with either an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB) can reduce the risk of diabetic nephropathy independent of their effect on BP. The degree of risk of CV events or progression to ESRD increases as albuminuria levels rise, and as eGFR falls, with the combination of albuminuria and low eGFR predicting a very high level of risk ( Figure 4 ) (53,54).
In type 1 diabetes, ACE inhibitors have been shown to decrease albuminuria and prevent worsening of nephropathy (59), and ARBs have been shown to reduce proteinuria (60). Blockers of the RAAS interfere with the kidney's response to intravascular volume contraction, namely, the ability of angiotensin II to contract the efferent arteriole to support glomerular filtration during these periods. In the case of severe renovascular disease that is bilateral (or unilateral in a person with a single functioning kidney), RAAS blockade can precipitate renal failure. Screening should commence at diagnosis of diabetes in individuals with type 2 diabetes and 5 years after diagnosis in adults with type 1 diabetes and repeated yearly thereafter. Pathological assessment reveals evidence of ischaemic injury and microvasculitis and prognosis is favourable. Report of a joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society. We place an emphasis on preventative medicine * and take an active role in maintaining your good health.
A variety of forms of kidney disease can be seen in people with diabetes, including diabetic nephropathy, ischemic damage related to vascular disease and hypertension, as well as other renal diseases that are unrelated to diabetes ( Figure 1 ) (7,8).
Initially, small amounts of albumin are leaked, below the detection threshold of a urine dipstick. While these biopsy series are biased (biopsies are usually done in people with diabetes when nondiabetic renal disease is suspected), other studies have suggested that half of everyone with diabetes and significant kidney function impairment do not have albuminuria (15). As the delay between onset and diagnosis of type 2 diabetes can be many years and as nondiabetic kidney disease is common, significant renal disease can be present at the time of diagnosis of type 2 diabetes (21,22), so screening should be initiated immediately at the time of diagnosis in this group. A random urine ACR predicts 24-hour urinary albumin excretion sufficiently well and is the test of choice for screening for albuminuria (23,25–27). Furthermore, diagnosing a person as having albuminuria requires the elevated urinary albumin level to be persistent. This equation requires knowledge of the patient's age, sex, serum creatinine and race and is automatically computed and reported by many labs whenever a serum creatinine is ordered. Because renal function can be transiently depressed, a persistent reduction in eGFR is required before it is considered to be abnormal. If either the eGFR remains low or at least 2 of the 3 random urine ACRs are abnormal, then a diagnosis of CKD is confirmed. This protective effect has been demonstrated in people with diabetes and hypertension (46) but not in normotensive people with diabetes (47–49). In type 2 diabetes, ACE inhibitors and ARBs have been shown to decrease albuminuria and prevent worsening of nephropathy, and ARBs have been shown to delay the time to dialysis in those with renal dysfunction at baseline (61–64). Nonsteroidal anti-inflammatory drugs cause constriction of the afferent arterioles, which can further reduce blood flow into the glomerulus in patients who are volume contracted. Myers Evolution of incipient nephropathy in type 2 diabetes mellitus Kidney Int 58 2000 1228 1237 Published erratum appears in Kidney Int. Pieringer Clinical versus histological diagnosis of diabetic nephropathy: is renal biopsy required in type 2 diabetic patients with renal disease?
Sharon The urine protein to creatinine ratio as a predictor of 24-hour urine protein excretion in type 1 diabetic patients with nephropathy. Lang Proteinuria, renal impairment, metabolic control, and blood pressure in type 2 diabetes mellitus.
Pogue Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients.
In this chapter, we will discuss how to screen for and diagnose chronic kidney disease (CKD) in people with diabetes, how to treat them with an aim to slow progression of CKD and discuss the impact of CKD on other aspects of diabetes management. These studies suggest that testing for albuminuria may be insufficient in identifying all patients with diabetes who have renal disease. At least 2 of 3 urine samples over time exhibiting elevations in urinary albumin levels are required before it is considered to be abnormal. A rapid decline in eGFR or development of severe hypertension would suggest prompt referral to a specialist.
The exception to this approach is when the random urine ACR indicates albuminuria in the overt nephropathy range, as this level of proteinuria rarely resolves spontaneously, so confirmatory testing is usually unnecessary. In type 2 diabetes, ACE inhibitors have also been shown to reduce the chance of developing new nephropathy (46,61). For these reasons, all of these drugs can reduce kidney function during times of intercurrent illness.
For these reasons, the serum creatinine and potassium should be checked between 1 and 2 weeks after initiation or titration of a RAAS blocker (82). In addition to measurements of urinary albumin excretion, estimations of the level of kidney function and urinalyses are required to identify patients with kidney disease other than diabetic nephropathy. Kidney diseases of all forms can be staged based on the degree of impairment of eGFR (Table 4 ). These renal-protective effects also appear to be present in proteinuric individuals with diabetes and normal or near-normal BP. In patients in whom a significant change in creatinine or potassium is seen, further testing should be performed to ensure that these results have stabilized. In most cases, the risk of ESRD in diabetes does not appear to matter whether the renal diagnosis is one of diabetic nephropathy or an alternative diagnosis as management is the same (16).
ACE inhibitors have been shown to reduce progression of diabetic nephropathy in albuminuric normotensive individuals with both type 1 (65–68) and type 2 diabetes (69). A number of additional medications need to be dose adjusted in patients with renal dysfunction, so their usage and dosage should be reevaluated during periods where kidney function changes. Thus, significant renal dysfunction is not usually seen until late in the course of diabetic nephropathy (13).




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