DIABETIC

NEPHROPATHY
Group A1

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 OBJECTIVES
-Definition
-Etiology and risk factors
-Pathophysiology
-Diagnosis
-Treatment

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 DEFINITION
• Diabetic Nephropathy is a
subtype of nephrotic
syndrome.
• It’s a 2ry glomerulopathy
which mean that the
patient had DM then he
developed Diabetic
nephropathy therefore we
understand that there is 1ry
glomerulopathy which
mean that kidney is the 1st
affected organ in cases like
minimal change disease
focal segmental
glomerulosclerosis and
membranous nephropathy.

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 ETIOLOGY, RISK
FACTORS AND
SYMPTOMS
• Cause: The patient has DM for
10 years or more poorly
controlled
• Risk Factors:
1. HTN
2. Smoking
3. High blood cholesterol
4. Obesity
5. family history of diabetes and
kidney disease

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 PATHOPHYSIOLGY
Diabetic Nephropathy is a
chronic disease, it starts with
microalbuminuria then
proteinuria.
Causes of hypoproteinemia:
1. decrease intake.
2. Decrease synthesis.
3. Increase loss:
malabsorption syndrome
in gut and protein losing
nephropathy in kidney
Which can lead to edema
in return (today topic)

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PATHOPHYSIOLOGY
Pathogenesis:
Diabetes, which is hyperglycemia,
too much glucose can destroy
cells in the body proteins and fat
by non-enzymatic glycosylation
(glycation) damaging vessels
causing retinopathy neuropathy
nephropathy. Diabetes damages
the kidney vessels and renal
glomeruli and renal pelvis.
When diabetes damage renal
vessels cause:
1. Macrovascular disease:
hyaline arteriosclerosis
2. Microvascular disease:
thickening of capillary
basemen membrane In return
it increases the permeability of
vessels and tubular cells to the
proteins
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PATHOPHYSIOLOGY
When diabetes damage glomeruli
it can cause:
1. Osmotic damage to the
glomerular capillary endothelium
as the glucose turned to sorbitol
by aldose reductase and sorbitol
attracts water which causes
oncotic damage.
2. Thickening of capillary
basement membrane by
deposition of type IV collagen
3. Hyperfiltration which causes
diffuse mesangial sclerosis.
4. Nodular Glomerulosclerosis.
When diabetes damage renal
pelvis it can cause pyelonephritis
WHEN DIABETES DAMAGE GLOMERULI IT CAN CAUSE:

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1. OSMOTIC DAMAGE TO THE GLOMERULAR CAPILLARY ENDOTHELIUM AS THE GLUCOSE TURNED TO SORBITOL BY ALDOSE REDUCTASE AND SORBITOL ATTRACTS WATER WHICH CAUSES ONCOTIC DAMAGE.
2. THICKENING OF CAPILLARY BASEMENT MEMBRANE BY DEPOSITION OF TYPE IV COLLAGEN
3. HYPERFILTRATION WHICH CAUSES DIFFUSE MESANGIAL SCLEROSIS.
4. NODULAR GLOMERULOSCLEROSIS.

WHEN DIABETES DAMAGE RENAL PELVIS IT CAN CAUSE PYELONEPHRITIS

3. HYPERFILTRATION WHICH CAUSES DIFFUSE MESANGIAL SCLEROSIS.
4. NODULAR GLOMERULOSCLEROSIS.
WHEN DIABETES DAMAGE RENAL PELVIS IT CAN CAUSE PYELONEPHRITIS

Normal GFR Abnormal Hyperfiltration

3. HYPERFILTRATION WHICH CAUSES DIFFUSE MESANGIAL SCLEROSIS.

4. NODULAR GLOMERULOSCLEROSIS.
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WHEN DIABETES DAMAGE RENAL PELVIS IT CAN CAUSE PYELONEPHRITIS
 DIAGNOSIS
 Blood Tests:
1. Serum Creatinine: Elevated levels may indicate impaired kidney function.
2. Blood Urea Nitrogen (BUN): Increased levels may suggest kidney dysfunction.
3. Glomerular Filtration Rate (GFR): GFR is an important measure of kidney function, and a decreased GFR can indicate kidney damage.
 Urine Tests:
1. Urinalysis: Detects the presence of protein (albuminuria), blood, and other abnormalities in the urine. Persistent proteinuria is a key indicator of
diabetic nephropathy.
2. Microalbuminuria Testing: Measures small amounts of albumin in the urine, an early sign of kidney damage.
 Imaging Studies:
1. Ultrasound: Can help assess the size and structure of the kidneys, detect any abnormalities, and evaluate blood flow to the kidneys.
2. CT Scan or MRI: These imaging studies may be used in certain cases to provide more detailed information about the kidneys.
 Kidney Biopsy:In some cases, a kidney biopsy may be performed to assess the extent and type of kidney damage. This invasive procedure is
usually reserved for cases where the diagnosis is uncertain or when other kidney diseases are suspected.

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DIAGNOSIS
In LM: Diffuse
thickening of
capillary wall,
Diffuse
mesangial
sclerosis and
papillary
necrosis
In EM:
Podocyte
Fusion
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MANAGEMENT

TREATMENT: ACE ANGIOTENSIN SGLT2 INHIBITORS:

MANAGEMENT:
INHIBITORS: RECEPTOR BLOCKERS EMPAGLIFLOZIN:
CONTROL OF BP (ARBS):
ENALAPRIL: STARTING STARTING DOSE IS
AND DIABETES
DOSE IS OFTEN 2.5 TO 5 LOSARTAN: STARTING OFTEN 10 MG ONCE
MELLITUS MG ONCE OR TWICE DAILY. DOSE IS OFTEN 25 TO DAILY.
50 MG ONCE DAILY.
LISINOPRIL: STARTING CANAGLIFLOZIN:
DOSE IS OFTEN 5 TO 10 MG IRBESARTAN:
STARTING DOSE IS
ONCE DAILY STARTING DOSE IS
OFTEN 100 MG
OFTEN 75 TO 150 MG
ONCE DAILY.
ONCE DAILY.

IMMUNOSUPPRESSIVE AGENTS (FOR SPECIFIC CASES):

CORTICOSTEROIDS (E.G., PREDNISONE): DOSES VARY WIDELY AND
ARE OFTEN TAILORED TO THE SPECIFIC CONDITION AND PATIENT
RESPONSE.
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CYCLOSPORINE OR TACROLIMUS: DOSES ARE INDIVIDUALIZED
BASED ON THE PATIENT'S IMMUNOSUPPRESSIVE NEEDS.

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THANK YOU

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