Clinical Case History of a Patient with Chronic Kidney Disease: Clinical Examination, Diagnosis, and Treatment Rationale. Like a realistic clinical case presentation written as if you are a doctor presenting a patient to your professor.

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KDIGO 2024 chronic kidney disease guideline evaluation management executive summary

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Illustrative Clinical Case Presentation: Chronic Kidney Disease

This is a fictional academic case, written in a ward-presentation format. It is not a substitute for assessment of an actual patient.

Good morning, Professor. I am presenting Mr. R.K., a 59-year-old man with progressive chronic kidney disease, most likely secondary to diabetic kidney disease and hypertensive nephrosclerosis.

1. Identification and chief complaints

Mr. R.K. is a 59-year-old male school administrator with known type 2 diabetes mellitus for 17 years and hypertension for 12 years. He presented with:

Progressive bilateral pedal edema for 2 months
Easy fatigability and reduced exercise tolerance for 6 weeks
Nocturia, about 4 to 5 times nightly
Reduced appetite and intermittent nausea for 2 weeks

He denies fever, dysuria, loin pain, gross hematuria, frothy urine noticed by the patient, skin rash, joint pain, or recent reduction in urine volume.

2. History of presenting illness

The patient had been reasonably well until approximately six months earlier, when he began noticing increasing tiredness. Over the preceding two months, he developed painless, pitting swelling of both ankles that is worse by evening. He reports a 3 kg weight gain during this period.

His diabetic control has been poor. He admits missing medications and dietary advice regularly. His most recent HbA1c was 9.1%. He was prescribed metformin and premixed insulin but often omitted insulin doses. He has never had documented diabetic retinopathy screening in the past three years.

He has hypertension treated intermittently with losartan 50 mg daily. Previous clinic records show blood pressure readings between 150/90 and 170/100 mmHg. He occasionally self-medicated with over-the-counter ibuprofen for knee pain, approximately 3 to 4 days per week for several months.

There is no history suggestive of acute nephritic syndrome, urinary obstruction, recurrent urinary tract infection, renal stones, autoimmune disease, hepatitis, HIV, or exposure to herbal medications.

3. Past history

Type 2 diabetes mellitus for 17 years
Hypertension for 12 years
Diabetic peripheral neuropathy
Dyslipidemia
No prior myocardial infarction, stroke, or heart failure
No known chronic liver disease or tuberculosis
No past dialysis, renal transplant, or renal surgery

Drug history

Metformin 1 g twice daily
Premixed insulin, inconsistently used
Losartan 50 mg daily, poor adherence
Atorvastatin 20 mg nightly
Intermittent ibuprofen use

Family and personal history

There is no family history of polycystic kidney disease or early kidney failure. He does not smoke and drinks alcohol occasionally. His diet is high in processed foods, salt, and refined carbohydrates. There is no known drug allergy.

4. Clinical examination

General examination

The patient was conscious, oriented, and mildly pale.

Parameter	Finding
Temperature	36.8°C
Pulse	84/min, regular
Blood pressure	166/94 mmHg, right arm seated
Respiratory rate	18/min
Oxygen saturation	98% on room air
Weight	81 kg
BMI	29.0 kg/m²

Other findings:

Mild conjunctival pallor
Bilateral pitting pedal edema up to the lower third of both legs
No icterus, cyanosis, clubbing, lymphadenopathy, or skin rash
No features of volume-overload pulmonary edema at presentation

Systemic examination

Cardiovascular system:
Normal first and second heart sounds. No murmur, gallop rhythm, or raised jugular venous pressure.

Respiratory system:
Bilateral vesicular breath sounds. No basal crepitations.

Abdominal examination:
Soft and non-tender. Kidneys were not ballotable. No palpable urinary bladder, ascites, hepatosplenomegaly, or renal bruit.

Neurologic examination:
Distal symmetrical reduction in vibration sensation and ankle reflexes, consistent with diabetic peripheral neuropathy. No focal neurologic deficit.

Fundus examination:
Non-proliferative diabetic retinopathy was present, supporting long-standing microvascular diabetic disease.

5. Investigations

Initial laboratory findings

Test	Result	Interpretation
Serum creatinine	3.0 mg/dL	Significantly elevated
eGFR	24 mL/min/1.73 m²	CKD G4 category
Blood urea nitrogen	58 mg/dL	Elevated
Urine albumin-creatinine ratio	860 mg/g	Severely increased albuminuria, A3
Urine routine microscopy	3+ protein, no active sediment	Supports chronic proteinuric kidney disease
Hemoglobin	9.8 g/dL	Anemia
MCV	88 fL	Normocytic anemia
Ferritin	60 ng/mL	Low iron stores for CKD
Transferrin saturation	16%	Iron deficiency contributing to anemia
Potassium	5.6 mmol/L	Mild hyperkalemia
Serum bicarbonate	18 mmol/L	Metabolic acidosis
Corrected calcium	8.4 mg/dL	Low-normal
Phosphate	5.4 mg/dL	Hyperphosphatemia
Intact PTH	380 pg/mL	Secondary hyperparathyroidism
HbA1c	9.1%	Poor glycemic control
LDL cholesterol	128 mg/dL	Above desirable level in high cardiovascular-risk CKD

Imaging

Ultrasound abdomen and kidneys

Right kidney: 9.3 cm
Left kidney: 9.5 cm
Increased bilateral cortical echogenicity
Poor corticomedullary differentiation
No hydronephrosis, stones, or renal mass
Bladder normal with insignificant post-void residual urine

The small echogenic kidneys support chronic irreversible parenchymal disease rather than acute kidney injury alone.

Cardiac evaluation

ECG: Sinus rhythm with no hyperkalemic ECG changes
Echocardiography: Mild concentric left ventricular hypertrophy; preserved ejection fraction

6. Problem representation

This is a 59-year-old man with long-standing poorly controlled type 2 diabetes and hypertension, severe albuminuria, progressive reduction in eGFR, diabetic retinopathy, and small echogenic kidneys, with complications including edema, hypertension, anemia, hyperkalemia, metabolic acidosis, and CKD-mineral and bone disorder.

7. Differential diagnosis

Diabetic kidney disease
Most likely because of long-standing diabetes, marked albuminuria, diabetic retinopathy, progressive decline in renal function, and absence of an active urinary sediment.
Hypertensive nephrosclerosis
Likely contributes because of long-standing inadequately controlled hypertension and echocardiographic left ventricular hypertrophy.
Chronic glomerulonephritis
Less likely because there is no hematuria, red-cell casts, systemic inflammatory feature, or nephritic presentation.
Obstructive uropathy
Unlikely because ultrasound showed no hydronephrosis or bladder outlet obstruction.
Analgesic-associated chronic tubulointerstitial injury
NSAID exposure may have accelerated renal decline but is unlikely to be the primary diagnosis.

8. Final diagnosis

Chronic kidney disease, G4A3, most likely due to diabetic kidney disease with hypertensive nephrosclerosis, complicated by:

Uncontrolled hypertension
Volume expansion with peripheral edema
Anemia of chronic kidney disease with iron deficiency
Mild hyperkalemia
Metabolic acidosis
CKD-mineral and bone disorder with hyperphosphatemia and secondary hyperparathyroidism
High cardiovascular risk
Poorly controlled type 2 diabetes mellitus

CKD is defined by persistent reduction in GFR and/or evidence of kidney damage. Diabetes and hypertension are the leading reported causes, while hypertension, proteinuria, and recurrent acute kidney injury are major drivers of progression. National Kidney Foundation Primer on Kidney Diseases, 8e, p. 524.

9. Treatment plan and rationale

A. Immediate measures

1. Stop nephrotoxins

Stop ibuprofen and advise avoidance of all non-steroidal anti-inflammatory drugs.
Review all prescription and non-prescription medications for nephrotoxicity and renal dose adjustment.
Avoid iodinated contrast unless essential and renal-protective precautions are used.

Rationale: NSAIDs may reduce renal perfusion, worsen hypertension and edema, precipitate hyperkalemia, and accelerate loss of residual kidney function.

2. Manage volume overload and hypertension

Restrict dietary sodium to less than 2 g sodium daily, approximately less than 5 g salt daily.
Start or optimize a loop diuretic, for example furosemide, with dose titration according to weight, edema, blood pressure, kidney function, and electrolytes.
Add amlodipine if blood pressure remains uncontrolled.
Encourage daily home blood-pressure and body-weight monitoring.

Rationale: Hypertension and proteinuria drive CKD progression. The KDIGO guideline suggests a standardized office systolic BP target below 120 mmHg when tolerated, with less intensive lowering in frail patients or those with symptomatic postural hypotension. It also supports sodium intake below 2 g/day in CKD. See the KDIGO 2024 executive summary.

B. Kidney-protective therapy

3. Continue renin-angiotensin system blockade cautiously

Continue losartan, if tolerated, and ultimately titrate toward the maximally tolerated dose after addressing potassium and monitoring renal function.
Check serum creatinine and potassium within 2 to 4 weeks after initiation or dose escalation.
Do not combine an ACE inhibitor with an ARB.

Rationale: He has diabetes with severely increased albuminuria. ACE inhibitors or ARBs lower intraglomerular pressure and albuminuria and slow progression of proteinuric CKD. KDIGO recommends renin-angiotensin system inhibitors in diabetic CKD with moderately to severely increased albuminuria, while avoiding ACE inhibitor plus ARB combination therapy. The guideline also advises that ACE inhibitor or ARB therapy may be continued even when eGFR falls below 30 mL/min/1.73 m² if clinically tolerated. See the KDIGO CKD recommendations.

Clinical caution: In this patient, potassium is already 5.6 mmol/L. The ARB should not be reflexively stopped, but potassium must be actively managed and monitored.

4. Start an SGLT2 inhibitor if no contraindication

Start dapagliflozin 10 mg daily or empagliflozin 10 mg daily, after reviewing volume status, infection history, ketoacidosis risk, and affordability.
Provide sick-day advice: temporarily withhold during prolonged fasting, major surgery, critical illness, severe dehydration, or suspected ketoacidosis.

Rationale: SGLT2 inhibitors reduce CKD progression and cardiovascular events in diabetic CKD. KDIGO recommends an SGLT2 inhibitor in adults with type 2 diabetes, CKD, and eGFR at least 20 mL/min/1.73 m². A small early reversible fall in eGFR can occur and is generally not a reason to discontinue therapy. See the KDIGO SGLT2 guidance.

5. Adjust diabetes treatment

Discontinue metformin because his eGFR is below 30 mL/min/1.73 m².
Continue insulin with individualized dose adjustment and frequent glucose monitoring because insulin clearance decreases in advanced CKD.
Refer for diabetes education and dietetic support.
Consider a GLP-1 receptor agonist if glycemic and weight targets remain unmet and there is no contraindication.

Rationale: The target is safe glycemic control without hypoglycemia, rather than aggressively normalizing glucose in advanced CKD.

C. Management of CKD complications

6. Hyperkalemia

Repeat potassium promptly to exclude sample hemolysis.
Obtain ECG if potassium increases, symptoms develop, or there is concern for cardiac effects.
Stop NSAIDs, correct acidosis, use a loop diuretic if volume expanded, and advise individualized restriction of high-potassium processed foods and salt substitutes.
Consider a chronic potassium binder if potassium remains elevated and is limiting kidney-protective RAAS blockade.

Rationale: There are no ECG changes and hyperkalemia is mild, so emergency dialysis is not indicated. However, recurrent or worsening hyperkalemia must be addressed because it can become life-threatening and may otherwise force withdrawal of beneficial RAAS inhibition.

7. Metabolic acidosis

Start oral sodium bicarbonate, with dose titrated to bicarbonate level, blood pressure, edema, and sodium load.
Monitor serum bicarbonate, sodium, potassium, body weight, and volume status.

Rationale: Correcting persistent metabolic acidosis may reduce muscle catabolism and help limit CKD-related complications. Care is needed because sodium bicarbonate can worsen hypertension or edema.

8. Anemia of CKD

Investigate anemia fully: repeat CBC, reticulocyte count, ferritin, transferrin saturation, vitamin B12, folate, and assess occult blood loss where indicated.
Give iron replacement, preferably intravenous iron in this advanced CKD patient with low transferrin saturation and significant anemia.
If hemoglobin remains below approximately 10 g/dL after iron repletion and reversible causes are excluded, consider an erythropoiesis-stimulating agent under nephrology supervision.
Avoid unnecessary blood transfusion, especially if renal transplantation may later be considered.

Rationale: CKD anemia is typically normocytic and multifactorial. Reduced endogenous erythropoietin production is a central mechanism, but iron deficiency, inflammation, blood loss, nutritional deficiency, hemolysis, and drugs must also be considered. Brenner and Rector’s The Kidney, 2-volume set, p. 2469.

9. CKD-mineral and bone disorder

Advise dietary phosphate reduction, especially processed foods containing phosphate additives.
Start a phosphate binder if phosphate remains elevated after dietary intervention.
Measure 25-hydroxyvitamin D and correct deficiency.
Follow serial calcium, phosphate, alkaline phosphatase, and PTH values rather than treating a single PTH value in isolation.
Involve nephrology before deciding on active vitamin D analogues or calcimimetic therapy.

Rationale: Reduced kidney function disrupts phosphate excretion, vitamin D activation, calcium balance, and PTH regulation, producing secondary hyperparathyroidism and CKD-mineral and bone disorder.

D. Cardiovascular risk reduction

Intensify statin therapy, if tolerated.
Encourage smoking avoidance, weight reduction, regular safe physical activity, vaccination, and dietary counselling.
Screen for ischemic heart disease and heart failure if symptoms emerge.

Rationale: CKD substantially increases cardiovascular risk. CKD care should reduce both kidney-failure progression and cardiovascular events. General disease-modifying strategies include RAAS blockade, SGLT2 inhibition, blood-pressure control, reduction of albuminuria, and cardiovascular risk reduction. National Kidney Foundation Primer on Kidney Diseases, 8e, p. 524.

10. Renal replacement therapy planning

This patient does not require urgent dialysis at present because he has:

No refractory pulmonary edema
No severe refractory hyperkalemia
No severe acidemia unresponsive to medical treatment
No uremic pericarditis, encephalopathy, or uncontrolled uremic symptoms
No dialysis-requiring intoxication

However, because he has CKD G4 with heavy albuminuria, he requires early nephrology referral for:

Kidney failure risk prediction
Education on hemodialysis, peritoneal dialysis, conservative kidney management, and transplantation
Timely vascular-access assessment if progression continues
Pre-emptive transplant evaluation where appropriate

Dialysis should be based on symptoms, complications, refractory metabolic abnormalities, fluid status, nutritional decline, and overall clinical condition, not eGFR alone.

11. Follow-up plan

Review in 1 to 2 weeks after medication changes.
Monitor blood pressure, weight, edema, serum creatinine, eGFR, potassium, and bicarbonate.
Repeat hemoglobin and iron studies after iron therapy.
Monitor calcium, phosphate, PTH, and vitamin D serially.
Measure urine ACR and eGFR at intervals determined by risk and trajectory.
Arrange nephrology, diabetic eye, foot-care, dietetic, and cardiovascular-risk follow-up.

KDIGO advises confirming reduced eGFR or albuminuria and using both urine albumin measurement and GFR assessment for CKD evaluation. It also recommends validated kidney-failure risk prediction in CKD G3 to G5. See the KDIGO 2024 guideline overview.

One-minute oral summary

Mr. R.K. is a 59-year-old man with poorly controlled long-standing diabetes and hypertension who has CKD G4A3, most likely diabetic kidney disease with hypertensive nephrosclerosis. He has nephrotic-range-range albuminuria, anemia with iron deficiency, hyperkalemia, metabolic acidosis, CKD-mineral and bone disorder, hypertension, and peripheral edema. Management priorities are removal of nephrotoxins, blood-pressure and volume control, continued monitored ARB therapy, addition of an SGLT2 inhibitor, adjustment of diabetic therapy, correction of anemia, acidosis and mineral-bone complications, cardiovascular-risk reduction, and early preparation for kidney replacement therapy if progression continues.

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