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The chapter includes a new algorithm for screening for chronic kidney disease in adults (Figure 1).
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. In addition, quantitative urinalysis tests may be performed to help diagnose many specific disorders, such as endocrine diseases, bladder cancer, osteoporosis, and porphyrias (a group of disorders caused by chemical imbalance).
Label the container with your name, the date, the time of completion, and return it as instructed.
This procedure may take a couple of attempts — lively infants can move the bag, causing the urine to be absorbed by the diaper. Deliver it to the laboratory or your health care provider as soon as possible upon completion. A clean catch is a method of collecting a urine sample for various tests, including urinalysis and urine culture. To obtain a clean-catch urine sample, boys and men should wipe the head of the penis clean. To perform this test, first urinate a small amount into the toilet bowl to clear the urethra of any contaminants.
For infants, the genital area is cleaned and dried, and then a collection device is attached to collect the urine. Routine urinalysis consists of three testing groups: physical characteristics, biochemical tests, and microscopic evaluation. The physical tests measure the color, transparency (clarity), and specific gravity of a urine sample. Biochemical testing of urine is performed using dry reagent strips, often called dipsticks. Additional tests are available for measuring the levels of bilirubin, protein, glucose, ketones, and urobilinogen in urine.
Blood: Red cells and hemoglobin may enter the urine from the kidney or lower urinary tract. Specific gravity: Specific gravity is a measure of the ability of the kidneys to concentrate urine by conserving water. Nitrite: Some disease bacteria, including the lactose-positive Enterobactericeae, Staphylococcus, Proteus, Salmonella, and Pseudomonas are able to reduce nitrate in urine to nitrite. Urobilinogen: Urobilinogen is a substance formed in the gastrointestinal tract by the bacterial reduction of conjugated bilirubin. Leukocytes: The presence of white blood cells in the urine usually signifies a urinary tract infection, such as cystitis, or renal disease, such as pyelonephritis or glomerulonephritis. A urine sample may contain cells that originated in the blood, the kidney, or the lower urinary tract.
The presence of bacteria or yeast and white blood cells helps to distinguish between a urinary tract infection and a contaminated urine sample.
The microscopic examination also identifies both normal and abnormal crystals in the sediment. Progression of diabetic nephropathy can be slowed through the use of medications that disrupt the renin-angiotensin-aldosterone system. 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 (13,14) ].
Role of blood pressure targets and specific antihypertensive agents used to prevent diabetic nephropathy and delay its progression. Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes.
Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy.

The effect of irbesartan on the development of diabetic nephropathy in patients with type 2 diabetes. The beneficial effect of angiotensin-converting enzyme inhibition with captopril on diabetic nephropathy in normotensive IDDM patients with microalbuminuria.
Should all patients with type 1 diabetes mellitus and microalbuminuria receive angiotensin-converting enzyme inhibitors?
Long-term stabilizing effect of angiotensinconverting enzyme inhibition on plasma creatinine and on proteinuria in normotensive type II diabetic patients. Microalbuminuria reduction with valsartan in patients with type 2 diabetes mellitus: a blood pressure-independent effect. Cardiovascular and renal outcomes with telmisartan, ramipril, or both in people at high renal risk: results from the ONTARGET and TRANSCEND studies.
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). 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) ]. A routine urinalysis usually includes the following tests: color, transparency, specific gravity, pH, protein, glucose, ketones, blood, bilirubin, nitrite, urobilinogen, and leukocyte esterase. Open a urine collection bag (a plastic bag with an adhesive paper on one end), and place it on the infant.
If you are asked to collect the urine, be sure the collection device is attached securely to prevent leakage.
The specific gravity of urine is a measure of the concentration of dissolved solutes (substances in a solution), and it reflects the ability of the kidneys to concentrate the urine (conserve water).
A urine dipstick consists of a white plastic strip with absorbent microfiber cellulose pads attached to it.
In general, these individual tests provide greater sensitivity; they therefore permit detection of a lower concentration of the respective substance.
These ketones are produced in excess in disorders of carbohydrate metabolism, especially Type 1 diabetes mellitus.
Testing for blood in the urine detects abnormal levels of either red cells or hemoglobin, which may be caused by excessive red cell destruction, glomerular disease, kidney or urinary tract infection, malignancy, or urinary tract injury. Most of the bilirubin produced in humans is conjugated by the liver and excreted into the bile, but a very small amount of conjugated bilirubin is reabsorbed and reaches the general circulation to be excreted in the urine. A positive test for nitrite indicates bacteruria, or the presence of bacteria in the urine. Increased urinary urobilinogen occurs in prehepatic jaundice (hemolytic anemia), hepatitis, and other forms of hepatic necrosis that impair the circulation of blood in the liver and surrounding organs. Microscopic examination of urinary sediment can provide valuable clues regarding many diseases and disorders involving these systems. Abnormal crystals are those formed as a result of an abnormal metabolic process and are always clinically significant.
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. 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. Some laboratories include a microscopic examination of urinary sediment with all routine urinalysis tests. The urinary microalbumin test measures the rate of albumin excretion in the urine using laboratory tests.

Your doctor may give you a special clean-catch kit that contains a cleansing solution and sterile wipes. Specific gravity is usually measured by determining the refractive index of a urine sample (refractometry) or by chemical analysis. The glomerulus is the network of capillaries in the kidneys that filters low molecular weight solutes such as urea, glucose, and salts, but normally prevents passage of protein or cells from blood into filtrate. Consequently, glycosuria (glucose in the urine) may be the first indicator that diabetes or another hyperglycemic condition is present. The urobilinogen test is helpful in differentiating these conditions from obstructive jaundice, which results in decreased production of urobilinogen.
The presence of cellular casts (casts containing RBCs, WBCs, or epithelial cells) identifies the kidneys, rather than the lower urinary tract, as the source of such cells.
Normal crystals are formed from normal metabolic processes; however, they may lead to the formation of renal calculi, or kidney stones. 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.
If not, it is customary to perform the microscopic exam, if transparency, glucose, protein, blood, nitrite, or leukocyte esterase is abnormal.
Normal conditions giving rise to turbid urine include precipitation of crystals, mucus, or vaginal discharge.
The person performing the test dips the strip into the urine, lets it sit for a specified amount of time, and compares the color change to a standard chart.
Albuminuria occurs when the glomerular membrane is damaged, a condition called glomerulonephritis. The glucose test may be used to screen newborns for galactosuria and other disorders of carbohydrate metabolism that cause urinary excretion of a sugar other than glucose. Bilirubin in the urine is derived from the liver, and a positive test indicates hepatic disease or hepatobiliary obstruction. 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). For example, red urine may be caused by blood or hemoglobin, beets, medications, and some porphyrias. It will be increased (above 1.035) in persons with diabetes mellitus and persons taking large amounts of medication.
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. Black-gray urine may result from melanin (melanoma) or homogentisic acid (alkaptonuria, a result of a metabolic disorder).
It will also be increased after radiologic studies of the kidney owing to the excretion of x ray contrast dye.
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. Consistently low specific gravity (1.003 or less) is seen in persons with diabetes insipidus. Thus, significant renal dysfunction is not usually seen until late in the course of diabetic nephropathy (13).
Orange urine may be caused by some medications or excessive urobilinogen (chemical relatives of urobilinogen). Urine volume below 400 mL per day is considered oliguria (low urine production), and may occur in persons who are dehydrated and those with some kidney diseases. Brown urine may be caused by excessive amounts of prophobilin or urobilin (a chemical produced in the intestines). A volume in excess of 2 liters (slightly more than 2 quarts) per day is considered polyuria (excessive urine production); it is common in persons with diabetes mellitus and diabetes insipidus.

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