CASE 2

A 46-years old woman presents to the clinic for the first time,
complaining of decreased urinary output for 5 months with a foamy
appearance. She also complain of swelling in both leg and none bloody,
non billious emesis a few times a week. She was diagnosed with diabetes
10 years ago. And has been taking insulin for two years. She does not
check her sugars at home because she does not like to stick herself. When
asked about her diet she states that she eats the best she can for what
she can afford but often has very little apetitte.
The patient last saw her physician 8 months ago. And insulin her
only medication. On examination, the patients is an obese woman. Her
temperature is 99F (37,2C), her heart 108beats/min, her blood pressure
is 198/105 mmHg, her respiration is 19 breaths/min, her oxygen
saturation is 94% on room air. A head, ears, eyes, nose, throat (HEENT)
examination reveal periorbital edema. Her skin is hyperpigmented on both
lower extremities. Her heart is tachycardi with an S1, S2, S4, gallop
ausculatated with no murmur or rub. When palpating the hearts point of
maximal impuls (PMI), it is lateral tp the left midclavicular line. There are
vesicular breath sound in both lungs throughout. Her neck reveals no
jugular venous distension and there are no carotid bruits. Her abdomen is
non tender, with no bruits or masses palpated. The lower extremities
reveal piting pretibial edema with a pit recovery time less than 40 second.
Laboratory studies in your office include a urinalysis showing hyaline
casts, 3+ proteinuria, and glucose, but negative for ketones. Her
hemoglobin is 10,9 gr/dl and her hematocryt is 32% with a mean
corpuscullar volume (MCV) of 82,3 gr/dl.

Keyword
-

A woman 46 years

Decresed urinary output for 5 months

Foamy appearance

Swelling in both legs & nonbloody

Nonbilious emesis a few times a week.

Has diabetes 10 years ago

Has been taking insulin for 2 years

Never check her sugar at home

Has bad eat behavior

Has very little appetite

Last time saw her physician 3 months ago

Insulin is her only medication

An obese woman

Physical examination &

investigation
-

An obese woman

Temperature is 99F (37,2C)

Heart rate : 108 beats/min

Blood pressure : 198/105 mmHg

Respiration : 19 breaths/min

O2 saturation : 94% on room air

HEENT : reveals periorbital edema

Skin : hyperpigmented on both lower extremities.

Heart : tachycardic with S1, S2, S4 gallop auscultated with no

murmur or rub

Palpating PMI : lateral to the left midclavicular line

Lung : vesicular breath sounds in both lungs throughout

Neck : no jugular venous distension, no carotid bruits

Abdomen : non tender, non bruits, no masses palpated

Extremities lower extremities : pitting edema, pit recovery time less

than 40 seconds.

Urinalysis : showing hyaline casts, 3+ proteinuria, glucose, ketones

(-).

Hb : 10,9 g/dL

Ht : 32% with mean corpuscillar volume (MCV) of 82,3 g/dL

Diagnose :

Diabetic Nephropathy

I.

Definition
Diabetic nephropathy is kidney disease or damage that can occur in
people with diabetes.

II.

Etiology
Each kidney is made of hundreds of thousands of small units called nephrons.
These structures filter your blood and help remove waste from your body.
In people with diabetes, the nephrons thicken and slowly become scarred over
time.

The kidneys begin to leak and protein (albumin) passes into the urine.
This damage can happen years before any symptoms begin.

The exact cause is unknown. However, kidney damage is more likely if

there is poor control of diabetes and high blood pressure.

In some cases, your family history may also play a role. Not everyone with
diabetes develops this kidney problem.
People with diabetes who smoke, and those with type 1 diabetes that started
before age 20 have a higher risk for kidney problems.

III. Symptom
Often, there are no symptoms as the kidney damage starts
and slowly gets worse. Kidney damage can begin 5 to 10 years
before symptoms start.
People who have more severe and long-term (chronic) kidney
disease may have symptoms such as:

Fatigue most of the time

General ill feeling

Headache

Nausea and vomiting

Poor appetite

Swelling of the legs

IV. Patophysiology
The key pathophysiologic event in diabetic nephropathy is
basement membrane damage.29 With renal damage, there is
progressive thickening of the basement membrane, pathologic
change in mesangial and vascular cells, formation of AGEs,
accumulation of polyols via the aldose reductase pathway,
and activation of protein kinase C.22,30,31 Passage of
macromolecules through the basement membrane may also
activate inflammatory pathways that contribute to the
damage secondarily.32
The renal hemodynamic abnormality is similar in type 1 and
type 2 diabetes.8 An early physiologic abnormality is
glomerular hyperfiltration33 associated with intraglomerular
hypertension.31 This is accompanied by the onset of
microalbuminuria, the first practical evidence of renal
involvement in diabetes. This is a critical time in the evolution
of diabetic renal disease, since the greatest impact of
treatment is to intercept this point in the otherwise inexorable
downward path of renal function.
A clinically asymptomatic period of decline follows, with
progression of microalbuminuria (30300 mg albumin per day)
to macroalbuminuria (>300 mg albumin per day). Once overt
nephropathy (macroalbuminuria) has developed, renal
function falls at a significant but variable rate (decline in GFR
of 220 ml/min/year). The rate of decline depends on type of
diabetes, genetic predisposition, glycemic control, and, very
importantly, blood pressure. Hypertension is the single most
important cause of progression and point of successful
intervention in diabetic nephropathy. Later stages may also be
accompanied by clinically significant albuminuria, edema, and
nephrotic syndrome. Eventually, the characteristic clinical
picture of renal failure develops.

V.

Risk Factor
Genetic susceptibility Genetic susceptibility may be an
important determinant of both the incidence and severity of
diabetic nephropathy
Blood pressure Studies have noted an association
between subsequent development of nephropathy and higher
systemic pressures, particularly if in the hypertensive range
The presence of these risk factors for hypertension is
particularly important in patients with relatively poor glucose

control (hemoglobin A1 concentration above 12 percent) are

at increased risk of overt nephropathy within 20 years.
Glycemic control Diabetic nephropathy is more likely to
develop in patients with lesser degrees of glycose control,
particularly if the hemoglobin A1c concentration is above 11
percent. Patients with type 1 diabetes whose hemoglobin A1c
concentration is maintained below 8.1 percent are at much
lower risk for renal disease.

VI. Investigation
VII. Treatment
Self-care.
Important treatments for kidney disease are tight control of
blood glucose and blood pressure. Blood pressure has a
dramatic effect on the rate at which the disease progresses.
Even a mild rise in blood pressure can quickly make kidney
disease worsen. Four ways to lower your blood pressure are
losing weight, eating less salt, avoiding alcohol and tobacco,
and getting regular exercise.
Drugs
When these methods fail, certain medicines may be able to
lower blood pressure. There are several kinds of blood
pressure drugs, however, not all are equally good for people
with diabetes. Some raise blood sugar levels or mask some of
the symptoms of low blood sugar. Doctors usually prefer
people with diabetes to take blood pressure drugs called ACE
inhibitors.
ACE inhibitors are recommended for most people with
diabetes, high blood pressure and kidney disease. Recent
studies suggest that ACE inhibitors, which include captopril
and enalapril, slow kidney disease in addition to lowering
blood pressure. In fact, these drugs are helpful even in people
who do not have high blood pressure.
Diet
Another treatment some doctors use with macroalbuminuria is
a low-protein diet. Protein seems to increase how hard the
kidneys must work. A low-protein diet can decrease protein
loss in the urine and increase protein levels in the blood.

Never start a low-protein diet without talking to your health

care team.

VIII.

Complication

hypoglycemia (due to decreased renal clearance of insulin)

rapidly progressing chronic kidney failure

end-stage kidney disease

hyperkalemia

severe hypertension

complications of hemodialysis

complications of kidney transplant

coexistence of other diabetes complications

peritonitis (if peritoneal dialysis used)

increased infections

IX. Prognosis
Diabetic nephropathy continues to get gradually worse.
Complications of chronic kidney failure are more likely to occur
earlier, and progress more rapidly, when it is caused by
diabetes than other causes. Even after initiation of dialysis or
after transplantation, people with diabetes tend to do worse
than those without diabetes.