Renal · Year 2 · from Renal
Case 1: Diabetic Nephropathy with Advanced CKD
Patient Presentation
Demographics: 62-year-old male
Chief Complaint: Progressive fatigue and decreased appetite for 3 months
History of Present Illness: The patient has a 20-year history of type 2 diabetes mellitus with poor glycemic control. He reports increasing fatigue, loss of appetite, mild nausea, and restless legs at night. He has noticed decreased urine output and mild bilateral lower extremity swelling. He denies gross hematuria or dysuria.
Past Medical History:
- Type 2 diabetes mellitus (HbA1c 9.2%)
- Hypertension (poorly controlled)
- Diabetic retinopathy
- Hyperlipidemia
Medications:
- Metformin 1000 mg twice daily
- Lisinopril 20 mg daily
- Amlodipine 10 mg daily
- Atorvastatin 40 mg daily
Physical Examination:
- Blood pressure: 158/94 mmHg
- Heart rate: 78 bpm
- General: Pale, appears fatigued
- Cardiovascular: S4 gallop, no murmurs
- Lungs: Clear to auscultation
- Abdomen: Soft, non-tender
- Extremities: 2+ pitting edema bilaterally
- Skin: Dry with mild excoriations from scratching
Workup and Results
Laboratory Studies:
- Creatinine: 3.8 mg/dL (baseline 1.4 mg/dL 2 years ago)
- BUN: 62 mg/dL
- eGFR: 14 mL/min/1.73m2
- Potassium: 5.6 mEq/L
- Bicarbonate: 18 mEq/L
- Phosphorus: 6.2 mg/dL
- Calcium: 8.2 mg/dL
- PTH: 285 pg/mL (elevated)
- Hemoglobin: 9.4 g/dL
- Albumin: 3.0 g/dL
- Urinalysis: 3+ protein, no blood
- Urine albumin-to-creatinine ratio: 2,400 mg/g
Renal Ultrasound:
- Bilateral kidneys 9.5 cm with increased echogenicity
- No hydronephrosis or masses
Clinical Image
Renal ultrasound demonstrating bilateral small, echogenic kidneys consistent with chronic kidney disease. The increased echogenicity reflects parenchymal fibrosis.
Diagnosis
Stage G5 Chronic Kidney Disease (ESKD) due to Diabetic Nephropathy with CKD-Mineral Bone Disorder and Anemia of CKD
- KDIGO Stage G5 (GFR <15 mL/min/1.73m2)
- Albuminuria Category A3 (>300 mg/g)
- CKD-MBD: Elevated PTH, hyperphosphatemia, hypocalcemia
- Anemia of CKD
Discussion
This case illustrates advanced diabetic nephropathy:
- Leading Cause of CKD: Diabetes mellitus accounts for 40-50% of CKD cases, as noted in the lecture. This patient has classic findings including heavy proteinuria, concurrent diabetic retinopathy, and gradually declining function over years.
- CKD Staging: Using KDIGO criteria, the patient has G5 disease (GFR <15) with A3 albuminuria (>300 mg/g). This combination places him at very high risk for progression and cardiovascular mortality.
- CKD-MBD Pathophysiology: The lecture describes how declining GFR leads to phosphate retention, decreased 1-alpha hydroxylase activity (low calcitriol), and secondary hyperparathyroidism. FGF-23 rises early as a compensatory phosphaturic hormone.
- Anemia: Decreased erythropoietin production from damaged kidneys is the primary mechanism. Target hemoglobin with ESA therapy is 10-11.5 g/dL.
- Uremic Symptoms: Fatigue, anorexia, nausea, restless legs, and pruritus represent uremic manifestations as toxins accumulate.
Treatment Plan
- Medication Adjustments:
- Discontinue metformin (contraindicated below GFR 30)
- Continue lisinopril for renoprotection (monitor potassium closely)
- Add SGLT2 inhibitor if tolerated
- CKD-MBD Management:
- Dietary phosphorus restriction (<800 mg/day)
- Sevelamer (non-calcium phosphate binder) with meals
- Calcitriol 0.25 mcg daily once phosphorus controlled
- Anemia Management:
- Iron studies to ensure adequate stores (ferritin >100, TSAT >20%)
- Erythropoietin-stimulating agent (ESA) initiation
- Metabolic Acidosis:
- Sodium bicarbonate supplementation (bicarbonate <22 mEq/L)
- ESKD Preparation:
- Nephrology referral for dialysis education (GFR <30)
- Arteriovenous fistula creation (should occur 6 months before anticipated dialysis)
- Transplant evaluation referral
Teaching Points
- Diabetes is the leading cause of CKD in developed countries
- KDIGO staging uses both GFR and albuminuria to stratify risk
- CKD-MBD involves phosphate retention, vitamin D deficiency, and secondary hyperparathyroidism
- Cardiovascular disease is the leading cause of death in CKD patients
- RAAS blockade and SGLT2 inhibitors provide renoprotection independent of diabetes status