DIABETIC NEPHROPATHY

Diabetic Nephropathy: Diagnosis,

Prevention, and Treatment
JORGE L. GROSS, MD MIRELA J. DE AZEVEDO, MD
SANDRA P. SILVEIRO, MD LUIS HENRIQUE CANANI, MD
MARIA LUIZA CARAMORI, MD THEMIS ZELMANOVITZ, MD

Diabetes Care 28:176 188, 2005

Diabetes Care 2016;39(Suppl. 1):S72S80 | DOI:
10.2337/dc16-S012

Background
Diabetic kidney disease occurs in 20
40% of patients with diabetes and is the
leading cause of end-stage renal disease
(ESRD)
At least once a year, assess urinary
albumin and estimated glomerular filtration
rate (GFR) in patients with diabetes
Early treatment delays or prevents the
onset of diabetic nephropathy/diabetic
kidney disease

Diabetic Nephropathy

Pathology
Non Enzymatic
Glycosylasion
AGE product
Colagen Syntesis

Hemodynamic Changes
GFR
Glomerular Capillary
Pressure

Changes In Kidney Structure & Function

Glomerular basement membrane (GBM)
width
Diffuse mesangial sclerosis
Hyalinosis, Microaneurysm, Hyaline
arteriosclerosis
Glomerulosclerosis Nodular (KimmelstielWilson )
Tubular Changes

Diagnosis
Screening for kidney damage (albuminuria) can be
most easily performed by urinary albuminto
creatinine ratio (UACR) in a random spot urine
collection.
Measurment of Albumin alone is less expensive but
susceptible to false-negative and false positive
determinations as a result of variation in urine
concentration due to hydration

Normal UACR :30 mg/g Cr

Diabetic Nephropathy
Stages

GFR
as a parameter of Kidney Function

Stages of CKD
Stages of CKD
Stag Description
e

GFR
(mL/min/1.73
m2)

Kidney Damage* with

normal or increased eGFR

90

Kidney Damage* with midly

decreased eGFR

60-89

Moderately decreased eGFR 30-59

4
Severely decreased eGFR
15-29
5
Kidney Failure
<15
Kidney damage is defined as abnormalities on
pathological, urine, blood or imaging tests

Prevention

Strategies and Goals

Treatment
Optimize glucose control to the risk or slow the
progression of diabetic kidney disease.
BP control to the risk or slow the progression of
diabetic kidney disease best choice : ACEinhibitor or ARB combined with spironolactone
Nondialysis-dependent diabetic kidney disease :
protein intake 0.8 g/kg/day
For patients on dialysis higher levels of dietary
protein intake
Either an ACE inhibitor or ARB is recommended for
patients with diabetes with UAE (30299 mg/day)
and 300 mg/day
and/or eGFR <60 mL/min/1.73 m2
Periodically monitor serum creatinine and potassium
if ACE inhibitors, ARB, or diuretics are used.

Treatmentcont
Continued monitoring of UACR in patients with
albuminuria treated with an ACE inhibitor or an
ARB
ACE inhibitor or an ARB is not recommended
for the primary prevention of diabetic kidney
disease in patients with diabetes who have
normal BP, normal UACR (<30 mg/g) & normal
eGFR
Referred for evaluation for renal replacement
treatment if they have eGFR<30 mL/min/1.73
m2
Refer to a physician experienced in the care of
kidney disease

Case Report
58-year-old man with a 13-year history of
type 2 DM visits a walk-in clinic because of
increasing swelling in his lower extremities.
The swelling began approximately 6 months
previously and has worsened over the past
6 weeks.
The patient reports no intercurrent illnesses
and sdenies any fever, chills, arthralgias,
joint swelling, or skin rash
He reports no visual changes, epistaxis,
hemoptysis, or cough, no symptoms of
flank pain, hematuria, dysuria, or darkening
of the urine.

History
The patients medical history is significant
for hypertension, type 2 DM.
His medications include glyburide 10 mg
daily, amlodipine 10 mg daily, and ibuprofen
occasionally.
He does not abuse alcohol, tobacco, or illicit
drugs.
No family history of kidney disease is
present, although several of his family
members have diabetes mellitus and heart
disease.

Physical Examination
BP is 152/93 mm Hg. HR is 75 bpm, RR is 14
breaths/min, and temperature is 37.3C
Examination of the head and neck is unremarkable,
with no evidence of conjunctivitis, lymphadenopathy,
thyromegaly
Examination of the fundi is notable for preproliferative
diabetic retinopathy.
The lungs are clear, the heart is remarkable for an S4
gallop.
Findings on abdominal examination are benign, with
no hepatosplenomegaly or palpable masses.
The lower extremities have 3+ pitting edema up to
the midcalf. No skin rash, petechiae, or purpura is
present
A neurologic examination is noncontributory, with no
focal findings or motor or sensory changes.

Work Up
The patients chest radiograph shows no
infiltrate, effusion, or adenopathy
24-hour urine collection confirms
nephrotic proteinuria (4.35 g of protein)
Work-up for secondary or systemic
causes of his renal disease is performed,
revealing no Anti DS-DNA, normal
complement and rheumatoid factor
levels, negative serology for hepatitis B
and C.

WORK UP

Biopsy
Light microscopic evaluation of the
kidney tissue is notable for
mesangial nodules
(ie, Kimmelstiel-Wilson nodules)
diffuse thickening of
capillary loops
and glomerulosclerosis

Discussion
What is the most likely cause of
the patients renal disease?
A)Diabetic nephropathy
B)Focal and segmental
glomerulonephritis
C)Light-chain deposition disease
D) Membranous glomerulonephritis
E)Minimal change disease

 What is the most appropriate

treatment?
A) Administer more amlodipine for better
control of blood pressure
B) Begin insulin therapy for better glycemic
control
C) Initiate therapy with an angiotensinconverting enzyme inhibitor
D) Restrict dietary protein to 0.6 g/kg body
weight per day
E) Strongly recommend a low-cholesterol diet