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Pregnancy in women with diabetic kidney disease

Authors
E Albert Reece, MD, PhD, MBA
Carol J Homko, RN, PhD, CDE
Matthew R Weir, MD
Section Editors
David M Nathan, MD
Michael F Greene, MD
Gary C Curhan, MD, ScD
Deputy Editor
Vanessa A Barss, MD, FACOG
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2015. | This topic last updated: Apr 27, 2015.
INTRODUCTION Women with either type 1 or type 2 diabetes mellitus can develop kidney
disease during their childbearing years [1]. It is usually due to classic diabetic nephropathy, the
major clinical manifestations of which are albuminuria and progressive chronic kidney disease
(CKD). CKD is defined by the presence of proteinuria, hematuria or decreased glomerular filtration
rate (GFR) for three or more months (table 1), irrespective of cause [2]. However, albuminuria in
diabetes mellitus is occasionally due to a glomerular disease other than diabetic nephropathy. In
women with diabetic kidney disease who become pregnant, the presence of kidney disease raises
important questions about the effects of the kidney disease on pregnancy outcome and the effects of
pregnancy on risk of progressive kidney dysfunction.
The management and outcome of pregnancy complicated by diabetic kidney disease will be
reviewed here. General issues pertaining to the pathogenesis and treatment of diabetic kidney
disease in nonpregnant individuals are discussed separately. (See "Overview of diabetic
nephropathy" and "Glycemic control and vascular complications in type 1 diabetes mellitus" and
"Treatment of diabetic nephropathy".)
LIMITATIONS OF AVAILABLE DATA There are many challenges in presenting and
interpreting the limited data available on pregnancy in women with diabetic kidney disease,
including:
The definitions/criteria for hypertension, albuminuria, and chronic kidney disease (CKD) have
been modified over time and much of the available data on pregnancy in women with diabetic
kidney disease predate these changes.
It is very difficult to make the diagnosis of preeclampsia in patients who enter pregnancy with
diabetic nephropathy, including hypertension and significant proteinuria. Escalation of both
hypertension and the quantity of protein in the urine is nearly universal in these women in the third
trimester, inevitably making the diagnosis of preeclampsia somewhat arbitrary in some or many
cases.
All of the data regarding treatment of hypertension in pregnant women with diabetic nephropathy
were reported in uncontrolled case series. Without controls, it is very difficult to separate the effects
of degree of blood pressure control from confounding factors associated with the degree of blood
pressure control. There are no randomized trials to provide guidance regarding choice of agents or
optimal blood pressure targets.

There have been many changes in general diabetes care, including strict metabolic control and
aggressive prepregnancy treatment of albuminuria and blood pressure, since the 1980s when many
of these studies were published. These changes in care may improve prognosis, but the effects of
the various interventions are very difficult to separate from one another.
EFFECT OF PREGNANCY ON DIABETIC KIDNEY DISEASE
Albuminuria Categories of albuminuria and proteinuria in nonpregnant adults have been defined
by Kidney Disease Improving Global Outcomes (KDIGO) (table 2) [2]. Normal pregnancy is
associated with an up to 60 percent increase in glomerular filtration rate (GFR) accompanied by a
modest decline in serum creatinine, and an increase in albuminuria excretion rate (see "Renal and
urinary tract physiology in normal pregnancy"). Similarly, in a study of 30 women with type 1
diabetes, but no kidney disease, albumin excretion rose almost four-fold to 43 mcg/min (equivalent
to 62 mg/day) [3].
In women with diabetic kidney disease, albuminuria also typically increases as pregnancy
progresses, and regresses to or near prepregnancy levels after delivery [4-6]. In a study of 12
women with moderately elevated albumin excretion rates of 30 to 300 mg/24 hours (formerly called
microalbuminuria) at baseline, urinary albumin excretion during pregnancy increased almost sevenfold to a mean of 492 mcg/min (equivalent to 708 mg/day), exceeding 3 g/day in four of the
women, but returning to baseline in all of the women within 12 weeks after delivery [3].
Kidney function In women with kidney disease (estimated GFR below 60 mL/min/1.73 m2 or
albuminuria), kidney function may decline during pregnancy (see "Pregnancy in women with
underlying renal disease", section on 'Effect of pregnancy on kidney disease'). Whether pregnancy
causes long-term worsening of diabetic kidney disease or hastens the progression to end-stage
kidney disease is controversial.
In nonpregnant patients with or without diabetes, serum creatinine above 1.5 mg/dL (132
micromol/L) and hypertension are the two major risk factors for progression of chronic kidney
disease (CKD). (See "Overview of the management of chronic kidney disease in adults", section on
'Natural history of renal disease' and "Overview of the management of chronic kidney disease in
adults", section on 'Slowing the rate of progression'.)
During pregnancy, there is concern that women with CKD who develop decreasing GFR, worsening
hypertension, and/or increasing proteinuria may be at risk of accelerated progression to end-stage
renal disease (ESRD) [7,8]. This concern is supported by three studies that examined the fall in
creatinine clearance in the years following pregnancy and found creatinine clearance decreased at
an average rate of 8 to 10 mL/minute/year [9-11]. This rate of decline is substantially higher than
the rate of decline (4 to 5 mL/minute/year) in nonpregnant diabetic patients with nephropathy on
renin-angiotensin-aldosterone system (RAAS) blockade [12,13].
However, diabetic women with normal albumin excretion or only albuminuria with normal GFR
appear to be at less risk for development or progression of kidney disease compared with those who
have reduced GFR. In the Diabetes Control and Complications Trial (DCCT), a multicenter
controlled clinical trial including 190 diabetic women who had 270 pregnancies and 500 diabetic
women who did not become pregnant, mean levels of albuminuria and proteinuria over a follow-up
period averaging 6.5 years were similar in both groups. Although this study did not enroll patients
with evidence of CKD, it suggests that pregnancy did not affect the long-term rate of development
of kidney disease [14]. The EURODIAB Prospective Complications Study (PCS) also found

pregnancy was not a risk factor for progression from normo- to microalbuminuria (ie, progression
of albumin excretion rate from 0 to 20 microg/mm to 20 to 200 microg/mm) [15].
However, permanent GFR loss or end-stage kidney disease may develop in women with poorly
controlled hypertension or CKD at the onset of pregnancy [8,16]. It appears that some of these
women require dialysis or kidney transplantation sooner than if they had not become pregnant. As
an example, in a study of 11 women in whom serum creatinine concentrations were 1.4 mg/dL
(124 micromol/L) at the onset of pregnancy, renal function remained stable in 27 percent,
transiently worsened in 27 percent, and permanently declined in 45 percent 6 to 57 months
postpartum [16]. Similar findings have been reported by others [6].
Although the number of women in these studies was small, accelerated decline in kidney function
has also been noted in pregnant women with CKD from causes other than diabetes. In one series of
76 women who had an initial mean plasma creatinine concentration of 1.9 mg/dL (168
micromol/L), 10 percent progressed to ESRD during pregnancy or immediately postpartum [17].
The risk of acceleration was highest among those with an initial plasma creatinine concentration
above 2.0 mg/dL (177 micromol/L), 33 versus 2 percent. (See "Pregnancy in women with
underlying renal disease", section on 'Effect on renal function'.)
EFFECT OF DIABETIC KIDNEY DISEASE ON PREGNANCY Perinatal morbidity and
mortality related to diabetic kidney disease have improved significantly in parallel with efforts to
achieve stringent glycemic control. Despite good glycemic control, chronic kidney disease (CKD) is
associated with an increased risk of a variety of pregnancy complications, including fetal growth
restriction, abnormal antenatal fetal assessment tests (nonreactive nonstress tests, low biophysical
profile scores), and preeclampsia. As a consequence, medically- or obstetrically-indicated preterm
delivery and cesarean birth are often required.
In the authors review of the world literature from 1981 to 1996 (figure 1 and figure 2), overall
perinatal survival in pregnancies complicated by diabetic kidney disease was 95 percent, compared
with approximately 99 percent survival in the general obstetric population [4]. Preterm delivery
occurred in 22 percent of pregnancies and was associated with significant neonatal morbidity (eg,
respiratory distress syndrome [20 percent] and jaundice [28 percent]). Fetal growth restriction
occurred in 15 percent of pregnancies. The overall congenital malformation rate was 8 percent.
Contemporary studies from the past decade have reported similar findings [18-22]. Although data
from randomized trials show that tight glycemic control during pregnancy correlated with reduced
rates of malformations [23], the clinical impact of this finding has not been substantial because of
the challenges in achieving euglycemia prior to conception, which is necessary to impart
measurable benefits on malformation rates [24-26].
The severity of CKD directly correlates with the risk of pregnancy complications [20,27-31], as
illustrated by the following examples:
In one study of 19 pregnancies in women with type 1 diabetes mellitus and nephropathy, the 11
women with preserved kidney function (ie, normal serum creatinine concentration) had less preterm
birth than the 6 women with moderate renal impairment (mean serum creatinine concentration
>1.87 mg/dL [165 micromol/L]) (median gestational age at delivery 36 4 weeks versus 31 3
weeks) [27].
In another series of 45 women with diabetic nephropathy, women with either moderately elevated
serum creatinine (>1.5 mg/dL [132.6 micromol/L]) or proteinuria >3 g/24 hours were at increased
risk of preterm delivery, low birth weight, and preeclampsia [28].

A study of women with diabetes with normal albumin excretion (albumin excretion rate <30
mg/24 hours, n = 203), albumin excretion rate 30 to 300 mg/24 hours (n = 26), and albumin
excretion rate >300 mg/24 hours (n = 11) reported preterm birth in 35, 62, and 91 percent,
respectively; small for gestational age infants in 2, 4, and 45 percent, respectively; and development
of preeclampsia in 6, 42, and 64 percent, respectively [31].
Preeclampsia is the most frequent complication of pregnancy in women with diabetic kidney
disease (in one review, preeclampsia developed in 35 to 66 percent of women with diabetes and
kidney disease versus 9 to 24 percent of women with diabetes and no kidney disease [32]). The risk
may be related, in part, to early pregnancy hypertension, level of kidney function, or level of
proteinuria.
In a large series by Coombs, et al evaluating the relationship between early-pregnancy proteinuria
and later development of preeclampsia (158 normotensive women and 49 women with chronic
hypertension), a receiver-operating characteristic curve showed an increased risk of preeclampsia in
women with early-pregnancy proteinuria 190 mg/day [33]. The rates of preeclampsia in women
with early-pregnancy proteinuria <190 mg/day (group 1), 190 to 499 mg/day (group 2), and 500
mg/day (group 3) were 7, 31, and 38 percent, respectively. This relationship persisted after adjusting
for the effects of parity, chronic hypertension, retinopathy, and glycemic control.
However, the low risk of preeclampsia in women with a low level of early pregnancy proteinuria
was not confirmed by a similar series published by How, et al 11 years later (including 141
normotensive and 52 hypertensive pregestational diabetics) [34]. In this series, the rates of
preeclampsia in women with early-pregnancy proteinuria of less than 190 mg/day (group 1), 190 to
499 mg/day (group 2), and 500 mg/day (group 3) were 17, 20, and 32 percent, respectively. There
was no significant difference in prevalence of preeclampsia between group 1 and group 2 and no
threshold that predicted development of preeclampsia. A similar relationship was evident in women
with chronic hypertension. The proportion of nulliparous women was similar in groups 1 and 2, but
higher in group 3. Glycemic control and presence of retinopathy were not considered in the
analysis.
The low prevalence of preeclampsia in group 1 of the Combs study [33] is comparable with that in
the nondiabetic population and is difficult to explain. Because neither the Combs study [33] nor the
How study [34] measured urine albumin excretion, it is possible that a higher proportion of group 1
women in the How study [34] had albumin excretion rates above normal, which is predictive of
development of preeclampsia (see below). The discordance could also relate to differences in
patient populations or undefined differences in diagnosis and management that have occurred over
the past decade.
However, in women with prepregnancy hypertension and CKD, it can be difficult to distinguish
preeclampsia from the physiological effects of pregnancy on blood pressure and albumin/protein
excretion, unless preeclampsia has severe features (eg, thrombocytopenia, elevated liver enzymes).
(See "Preeclampsia: Clinical features and diagnosis", section on 'Differential diagnosis'.)
MANAGEMENT PRINCIPLES Women with diabetes mellitus should be evaluated
preconception for complications of diabetes and glucose control should be assessed. At that time,
they should be counseled about the risk of adverse pregnancy outcome (eg, congenital
malformations, miscarriage, preeclampsia) and progression of diabetic kidney disease, and
interventions to minimize these risks. Ideally, pregnancy will be delayed until optimum maternal
medical status is achieved. Informed women are more motivated to adhere to intensive treatment
regimens.

The existence of a metabolic derangement appears to be the key factor mediating vascular
complications, not whether the patient has type 1 or type 2 diabetes [35-40]. Therefore, there is no
difference in the general approach to treating diabetic kidney disease in patients with or without
insulin-dependent disease. Diabetic kidney disease is not a contraindication for pregnancy;
however, most women with very high serum creatinine levels (ie, >2 or >3 mg/dL) are usually
subfertile [41-43]. If a patient with high serum creatinine does become pregnant, her pregnancy
does not accelerate the kidney disease, and the stage of the kidney disease would not harm the
pregnancy, provided that the patient is under intensive surveillance and management [44-46]. (See
"Pregestational diabetes: Preconception counseling, evaluation, and management" and
"Pregestational diabetes mellitus: Prenatal glycemic control".)
Treatment of hypertension During pregnancy, treatment of hypertension in women with diabetic
kidney disease appears to be associated with improved fetal outcome and a decrease in maternal end
organ damage [11,18,28,47,48]. Conversely, suboptimal control of hypertension in these women is
associated with a significant risk of preterm delivery [19]. Early and intensive initiation of
antihypertensive therapy appears to result in better pregnancy outcomes as compared with delayed
therapy [18]; therefore, we suggest timely initiation of therapy. These women should be managed
by an expert team including a maternal-fetal medicine specialist, diabetologist, and nephrologist
(especially if glomerular filtration rate [GFR] is decreased or serum creatinine concentration is >2
mg/dL at pregnancy onset).
In women with diabetic kidney disease, we suggest a blood pressure goal in line with the American
Diabetes Association recommendations for women with diabetes: target blood pressure goals of
systolic blood pressure 110 to 129 mmHg and diastolic blood pressure 65 to 79 mmHg during
pregnancy, as pressures in this range may benefit long-term maternal kidney function, and are
unlikely to impair fetal growth [49]. It is important to note, however, that the treatment goal needs
to be individualized, as there are no prospective studies examining blood pressure targets and no
data demonstrating that pregnant women with diabetic kidney disease have better outcomes with
this blood pressure goal.
We suggest use of nondihydropyridine calcium channel blockers, such as diltiazem and verapamil,
in women with albuminuria [50], given these drugs reduce both blood pressure and proteinuria.
Dihydropyridine calcium channel blockers, such as nifedipine or amlodipine, can also be used, but
may not be as effective in reducing proteinuria. Many women with diabetic kidney disease require a
combination of therapies to achieve adequate blood pressure control and reduce urine albumin
excretion. There are several reasonable options for additional antihypertensive therapy, including
methyldopa, beta blockers, hydralazine, clonidine, and thiazide diuretics [51-53]. Methyldopa has
been used safely for many years, but is only modestly effective and has sedating effects. Beta
blockers are a heterogenous class. Labetalol does not appear to affect uteroplacental blood flow, and
can be given orally or parenterally [54]; however, other beta blockers, particularly non-selective
beta blockers, have been associated with lower placental and fetal weight when used early in
pregnancy, myometrial relaxation, and premature labor [55-57]. Hydralazine has a good safety
profile in pregnancy, and can be given orally or parenterally [58], but can be associated with reflex
tachycardia and fluid retention. Clonidine has a similar mechanism of action to methyldopa. It can
be given orally or as a transcutaneous patch; abrupt discontinuation should be avoided, if possible,
as rebound increases in blood pressure can occur. Thiazide diuretic use during pregnancy is
controversial; volume depletion is unusual [59], but patients should be monitored for potential
changes in serum electrolytes. (See "Management of hypertension in pregnant and postpartum
women" and "Treatment of hypertension in patients with diabetes mellitus".)

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are
contraindicated during all stages of pregnancy because of teratogenic risk (see "Angiotensin
converting enzyme inhibitors and receptor blockers in pregnancy"). In contrast, in nonpregnant
women, these drugs are the treatment of choice for mitigation of proteinuria and chronic kidney
disease (CKD) progression in type 1 and type 2 diabetics, respectively (see "Moderately increased
albuminuria (microalbuminuria) in type 1 diabetes mellitus" and "Moderately increased albuminuria
(microalbuminuria) in type 2 diabetes mellitus"). In small observational studies, women treated
with ACE inhibitors and intensive metabolic control for three to six months before conception
maintained a renoprotective effect throughout pregnancy [60,61]. Prepregnancy treatment was also
associated with favorable perinatal outcomes. Preconception treatment with ACE inhibitors or
ARBs is appropriate preconception, but should be discontinued as soon as the pregnancy is
identified because of their well-demonstrated teratogenic effects, and safer anti-hypertensive drugs
should be initiated [62].
Prevention of preeclampsia As discussed above, women with diabetic kidney disease are at
increased risk of developing preeclampsia (see 'Effect of diabetic kidney disease on pregnancy'
above). Multiple professional organizations have recommended use of low-dose aspirin prophylaxis
for pregnant women at moderate to high risk of developing preeclampsia. A modest reduction in the
risk of preeclampsia is possible; however, we believe no prophylaxis is also reasonable, given that
experts have been unable to identify a group of pregnant women who will predictably derive a
clinically significant benefit from low-dose aspirin therapy and there is no consensus on criteria to
define women at moderate to high risk for preeclampsia. These data are reviewed in detail
separately. (See "Preeclampsia: Prevention", section on 'Antiplatelet agents'.)
Most of these data included women with various risk factors for preeclampsia. In one of the few
trials that included only diabetic women, 462 women with type 1 diabetes were randomly assigned
to receive either low-dose aspirin or placebo during pregnancy [63]. The rate of preeclampsia was
similar for the aspirin and the placebo groups (18.7 versus 21.7 percent; RR 0.87, 95% CI 0.601.25) and there was no difference in the rate of preeclampsia between aspirin and placebo for any of
the subgroups in the trial (diabetes with no hypertension or proteinuria, diabetes with proteinuria
only, diabetes with hypertension only, diabetes with both hypertension and proteinuria). As
discussed above, in women with prepregnancy hypertension and CKD, it can be difficult to
distinguish preeclampsia from the physiological effects of pregnancy on blood pressure and
albumin/protein excretion, unless preeclampsia has severe features (eg, thrombocytopenia, elevated
liver enzymes, cerebral or visual symptoms). (See "Preeclampsia: Clinical features and diagnosis",
section on 'Differential diagnosis'.)
Antenatal care Routine issues in the obstetrical management of pregnancies complicated by type
1 and type 2 diabetes are discussed separately. (See "Pregestational diabetes mellitus: Obstetrical
issues and management".)
In addition to standard obstetrical care, we recommend the following in women with diabetic
kidney disease:
Although there is no universal standard for how often a patients kidney function should be
monitored, many institutions measure urine albumin-to-creatinine ratio in an untimed urinary
sample at least monthly. This is the preferred method for evaluation of albuminuria. (See
"Moderately increased albuminuria (microalbuminuria) in type 1 diabetes mellitus", section on
'Detection' and "Moderately increased albuminuria (microalbuminuria) in type 2 diabetes mellitus",
section on 'Detection'.)

Serum creatinine can be used to estimate GFR in individuals with stable kidney function.
Intervention because of worsening kidney function (ie, falling creatinine clearance, increasing blood
pressure, development of uremia) is indicated if the intervention may have favorable maternal or
fetal consequences, and should be individualized for each patient [64]. (See "Assessment of kidney
function".)
Monitor blood pressure at least monthly. Antihypertensive drugs are administered or adjusted, as
needed, to maintain systolic blood pressure 110 to 129 mmHg and diastolic blood pressure 65 to 79
mmHg. Calcium channel blockers (particularly the non-dihydropyridines) are preferred; ACE
inhibitors and ARBs should not be used.
Home blood pressure monitoring should be encouraged. Although there are no data to indicate
improved outcomes with home monitoring in pregnant women, there is evidence in the general
population that home measurements of blood pressure are of value for evaluating adequacy of
treatment. Ambulatory blood pressure monitoring may also be helpful in gauging blood pressure
values, or response to therapy. (See "Blood pressure measurement in the diagnosis and management
of hypertension in adults", section on 'Home blood pressure monitoring'.)
Sonographic assessment of fetal growth every four to six weeks in the last half of pregnancy.
Diabetic kidney disease does not influence the management of intrauterine growth restriction or
macrosomia (estimated fetal weight >4500 grams), if present. (See "Shoulder dystocia: Risk factors
and planning delivery of at risk pregnancies", section on 'Planning delivery in at risk pregnancies'
and "Fetal growth restriction: Evaluation and management", section on 'Pregnancy management'.)
Fetal assessment with nonstress tests or biophysical profile score or a combination of these tests
twice per week is begun at 32 weeks, but may be initiated as early as 26 weeks in patients who
develop obstetrical indications for fetal assessment (eg, intrauterine growth restriction,
preeclampsia). (See "Overview of antepartum fetal surveillance".)
In obstetrically uncomplicated, medically stable women, there is no significant benefit of
expectant management beyond 390/7ths weeks of gestation. Earlier delivery in other clinical scenarios
should be decided on a case-by-case basis. (See "Preeclampsia: Management and prognosis" and
"Pregestational diabetes mellitus: Obstetrical issues and management", section on 'Timing of
delivery' and "Fetal growth restriction: Evaluation and management", section on 'Pregnancy
management'.)
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Basics topics (see "Patient information: Care during pregnancy for women with type 1 or type 2
diabetes (The Basics)")
Beyond the Basics topics (see "Patient information: Care during pregnancy for women with type 1
or 2 diabetes mellitus (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
In women with diabetic kidney disease, albuminuria typically increases as pregnancy progresses,
and regresses to or near prepregnancy levels after delivery. (See 'Albuminuria' above.)
Pregnant women with diabetes and normal albumin excretion are at low risk for development of
kidney disease. Pregnant women with diabetes, microalbuminuria, and normal kidney function
appear to be at low risk for loss of kidney function, but may have a transient increase in
albuminuria. However, women with poorly controlled hypertension or reduced glomerular filtration
rate (GFR) and increased proteinuria (serum creatinine level >1.5 mg/dL, proteinuria >3 g in 24
hours) at the onset of pregnancy are at risk of permanent kidney damage, including end-stage
kidney disease. (See 'Kidney function' above.)
Diabetic kidney disease is associated with an increased risk of pregnancy complications, including
fetal growth restriction, abnormal antenatal fetal assessment tests (nonreactive nonstress tests, low
biophysical profile scores), and preeclampsia, even in women with good glycemic control. The
occurrence of these pregnancy complications may necessitate preterm delivery and increases the
chance of cesarean birth. (See 'Effect of diabetic kidney disease on pregnancy' above.)
In women with diabetic kidney disease, we suggest a blood pressure goal in line with the
American Diabetes Association recommendations for pregnant women with diabetes: 110 to 129/65
to 79 mmHg. We suggest use of nondihydropyridine calcium channel blockers in the presence of
albuminuria (Grade 2C), given favorable effects on both blood pressure and proteinuria. (See
'Treatment of hypertension' above.)
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are
contraindicated during all stages of pregnancy because of teratogenic risk. (See "Angiotensin
converting enzyme inhibitors and receptor blockers in pregnancy".)
In women with chronic primary or secondary hypertension or previous pregnancy-related
hypertension, low-dose aspirin from the 12th week of gestation until delivery is suggested, but
should be determined on a case-by-case basis. (See "Preeclampsia: Prevention".)
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GRAPHICS
Definition and criteria for chronic kidney disease
Definition
Chronic kidney disease is defined based on the presence of either kidney damage or decreased
kidney function for three or more months, irrespective of cause.

Criteria

Comment
Duration is necessary to distinguish chronic from acute
kidney diseases.

Duration 3 months, based on


documentation or inference

Clinical evaluation can often suggest duration

Documentation of duration is usually not available in


epidemiologic studies

GFR is the best overall index of kidney function in health


and disease.

Glomerular filtration rate (GFR) <60


mL/min/1.73 m2

The normal GFR in young adults is approximately


125 mL/min/1.73 m2; GFR <15 mL/min/1.73 m2 is
defined as kidney failure

Decreased GFR can be detected by current estimating


equations for GFR based on serum creatinine
(estimated GFR) but not by serum creatinine alone

Decreased estimated GFR can be confirmed by


measured GFR

Pathologic abnormalities (examples). Cause is based on


underlying illness and pathology. Markers of kidney damage
may reflect pathology.

Kidney damage, as defined by


structural abnormalities or functional
abnormalities other than decreased
GFR

Glomerular diseases (diabetes, autoimmune diseases,


systemic infections, drugs, neoplasia)

Vascular diseases (atherosclerosis, hypertension,


ischemia, vasculitis, thrombotic microangiopathy)

Tubulointerstitial diseases (urinary tract infections,


stones, obstruction, drug toxicity)

Cystic disease (polycystic kidney disease)

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