This document presents a case study of a 53-year-old African American woman (Patient A) with a 17-year history of type 2 diabetes, hypertension, and hyperlipidemia who presents with shortness of breath, pruritus, and leg edema. Laboratory tests show abnormal kidney and liver function as well as poor diabetes control. The likely diagnosis is diabetic nephropathy based on her medical history and test results. Treatment goals should focus on improving blood pressure and glucose control as well as reducing albuminuria through medication changes and lifestyle modifications.
2. Diabetic nephropathy
Diabetic nephropathy (Diabetic kidney Disease DKD ) is a serious complication
of type 1 diabetes and type 2 diabetes.
Diabetic kidney disease is divided into two main categories, depending on how
much albumin is lost through the kidneys:
1. Microalbuminuria (incipient nephropathy): 30-300 mg per day
2. Macroalbuminuria (Proteinuria or overt nephropathy): <300 mg per day.
3. Hyperglycemia lead to the buildup of
extra material in the glomeruli, which
increases the force of the blood moving
through the kidneys and creates stress
in the glomeruli.
When the kidneys' filtering units
are damaged, albumin may be
able to pass through the filter and
into the urine.
At the onset of diabetes, blood
flow into the kidneys increases
which may strain and lessen the
ability of glomeruli to filter
This stress leads to gradual and
progressive scarring of the glomeruli,
eventually reducing the kidneys'
ability to filter blood properly.
01 02 03 04
Causes
6. Case study
Patient A is an African American woman, 53 years of age, with a 17-year history of type
2 diabetes, hypertension, and hyperlipidemia and a 35-year history of smoking. She had
been referred to a diabetes clinic for intensive diabetes self-management education and
training over this period. She presents in the office with shortness of breath, pruritus,
and pitting edema of bilateral extremities. Her blood pressure is 165/92 mm Hg, heart
rate 94 beats per minute (regular rate and rhythm), and respiration 26 breaths per minute.
She is 5 feet 3 inches tall and weighs 202 pounds (BMI: 35.8). Other physical
examination features, apart from leg edema, are unremarkable. Blood is taken and sent
to the laboratory for analysis, which reveals some abnormal findings.
1. Type-2 diabetes on metformin ER 1000mg
therapy
2. Hypertension with Lisinopril 40 mg twice a
day
3. Hyperlipidemia, on Atorvastatin 80 mg
daily.
4. CAD with history of stent placement on
Plavix 75mg daily (allergy from aspirin)
Past Medical History
8. 1- What is the likely diagnosis of patient A?
Diabetic nephropathy
2- What features in patient A’s case are consistent with this
diagnosis?
Hypertension.
Shortness of breath.
Pitting edema of bilateral extremities.
Albuminuria.
9. 3- What should be the goals of therapy?
Reduce Blood pressure to <130/80 mmHg
Maximal reduction of albuminuria
Treat hyperlipidemia (LDL <100 mg/dL)
Reduce HbA1c to ≤ 7.0%
Body mass index ≤ 25 kg/m?
Stable creatinine/eGFR
10. 4- What is the best next step for the treatment of hyperglycemia?
The patient was taking metformin, which is considered the best first-line
oral drug for patients with type 2 diabetes and normal kidney function
because of its low cost and beneficial all-cause and cardiovascular
mortality effects. It carries a low risk of hypoglycemia and has weight-
lowering properties. Metformin use for patients with eGFR<30 ml/min per
1.73𝑚2
should not be prescribed so In the patient presented, metformin
should be stopped
From the standard of medical care in diabetes the sodium glucose
cotransporter-2 (SGLT2) inhibitors is considered as first agent in chronic
kidney disease and albuminuria but would not be an option in this patient
as their efficacy is reduced and toxicity is more likely in patients with an
eGFR<30 ml/min per 1.73 𝑚2
11. So the next preferred glucose-lowering agent for patients with type 2
diabetes and CKD is a long-acting glucagon-like peptide 1 receptor
agonist (GLP1RA) because of benefits in chronic kidney disease and It
also reduces albuminuria and may slow eGFR decline.
Glucagon-like peptide 1 (GLP1) is an incretin hormone secreted from the
intestine after ingestion of nutrients that stimulates release of insulin from
the pancreas . GLP1 also slows gastric emptying and decreases appetite
stimulation. GLP1 receptor agonists stimulate this pathway to lower blood
glucose and body weight.
12. 5- The patient is on a maximum dose of an ACE inhibitor. What additional
pharmacotherapy can be given to further regress albuminuria and
improve outcome?
Combination therapy with an ACE inhibitor and an ARB with a direct renin
inhibitor (aliskiren) may further reduce proteinuria.
Plasma aldosterone levels are more elevated in a subset of patients after
initiation of ACE inhibitor or ARB therapy. This is called aldosterone
breakthrough, and it is thought to be due to increased renin.
aldosterone blockade using spironolactone or eplerenone with close
monitoring of serum potassium levels has an additive effect on reducing
proteinuria when combined with an ACE inhibitor or an ARB.
Novel MRAs, including finerenone (a nonsteroidal MRA with greater receptor
selectivity and affinity compared with steroidal MRAs), have been shown to
improve albuminuria in DKD when added to an ACE inhibitor or an ARB,
with a low incidence of hyperkalemia
13. 6- Mention the lifestyle intervention should be included in patient
diabetic educational program
lifestyle modifications, including exercise and weight loss (to
achieve 7% loss of initial body weight within 3months).
smoking cessation .
Nutritional counseling
14. Made by:
1. Rowaa Oraby Ali
2. Reem Amr Khafagy
3. Rowan Osama Fathy
4. Amira Mohamed Abdallah