Dr. NK Hase delivers a masterclass on kidney diseases, exclusive in this weekly series for M3 India. In the final part, he discusses 6 cases on kidney disease, writing in detail on the evaluation, aetiology, and final diagnosis. If you have queries, send in your questions at the end of this article. Dr. Hase will address them in a separate article, once this series concludes.

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Case 1

A male, 70 years of age presents with h/o urgency, frequency, precipitancy, and nocturia. He is non-diabetic, non-hypertensive, and there is no h/o burning, fever, suprapubic pain, straining, or poor/slow stream.

Physical examination: Pulse- 90/min; BP- 150/80 mmHg, otherwise unremarkable.

Urine: Protein absent, no RBC, WBC

Other evaluations: Serum creatinine is 0.8 mg, blood glucose is 80 mg, fasting HbA1c is 5.4%. S.Na is 138meq/l, S.K is 4.5meq/l, urine flow rate is 15 ml/sec. There is no bladder wall thickening or prostate enlargement.

Analysis

Does the patient have kidney disease? Yes

Where is the site of lesion? LUT most likely bladder

Aetiology: Overactive bladder

Symptoms are suggestive of storage function dysfunction, but normal renal function. Other possibilities are prostatic enlargement, or suprapontine brain lesion. Urine flow is normal and there is no h/o. Stroke, Parkinsonism most likely could cause overactive bladder.

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Case 2

A female, 9 years old reports with h/o puffiness of face, oedema in the feet, h/o passing cola-coloured urine, h/o fever, sore throat 2 days prior, and breathlessness on exertion.

Physical examination: Puffines of face; pallor+; pulse- 100/min; BP- 150/100 mmHg; oedema of the feet, RS- basal crepts; CVS- HS normal no murmur. Liver, spleen was not palpable.

Urine: Smoky, protein++, sugar was absent.

Other evaluations: RBC- 40 to 50/hpf (dysmorphic), BUN- 40 mg, serum creatinine- 1.8 mg/dl, S.Na- 135 meq/l, S. K- 5.8 meq/l, CL- 96 meq/l, HCO3- 12 meq/l, C3- 100, C25, ANA- negative, HbsAg/HCV- negative, USG revealed right kidney- 13 cm and left kidney- 12.5 cm.

Analysis

Does the patient have kidney disease? Yes

Where is the site of lesion?

Considering glomerular haematuria and proteinuria, it is glomerular lesion- acute nephritis (proliferative) glomerular disease. Possibilities include IgA, infection-related GN, vasculitis, SLE. As it complements normal aetiology, so it is most likely IgA nephropathy. When there is acute kidney injury, complications present such as azotemia, fluid overload, hyperkalemia, and metabolic acidosis. This patient will need kidney biopsy to confirm diagnosis of IgA Nephropathy.

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Case 3

A male, 34 years old farmer was referred for increased serum creatinine of 3.5 mg/dl. Six months back, it was 3.0 mg/dl. There was no h/o DM, HT and no h/o of oedema of the feet, puffiness of face, h/o nocturia, h/o polyuria, no h/o haematuria, no h/o nocturnal enuresis, no h/o straining for urine, no h/o renal stones, and no h/o NSAID intake.

Physical examination: Pulse- 80/min; BP- 110 mmHg, no oedema ,other system unremarkable,

Urine: Protein trace, Glucose +, no RBCs or WBCs, SP Gravity: 1005

Other evaluations: Hb- 7.00 g/dl; BUN- 30 mg/dL; serum creatinine- 3.2 mg/dl, S uric acid- 8.5 mg/dl, S. Na- 132 meq/l; K- 3.5 meq/l; Cl- 110; HCO3- 18, S.Ca- 7.5 mg/dl; PO4- 6.5 mg/dl; S. albumin- 2.5 g/dl; USG- right kidney 8.5 cm x 3.5 cm and left kidney 7.5 cm highly echogenic; PCS- normal

Analysis

Does the patient have kidney disease? Yes

Where is the site of lesion?

The patient most likely has tubulointerstitial lesion as he presented with azotemia, no diabetes, no hypertension, nocturia, polyuria, no significant proteinuria, low specific gravity urine, glucosuria. Acidosis normal AG suggests mainly tubule-interstitial rather than glomerular or vascular problem. Aetiology is not known. There is evidence of chronic kidney disease stage 4 (eGFR 24 ml/min). Complications include azotemia, anaemia, metabolic acidosis, hypokalemia hyperphosphatemia, and hypoalbuminaemia.

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Case 4

A female, 27 years old, married, was referred for hypertension BP 180/110 mmHg, with h/o headache on and off, fatigue, low grade fever, loss of appetite, giddiness, no puffiness of face, oedema, no haematuria, nocturia, no h/o urinary tract infections, no stones, one abortion.

Physical examination: P: 70/min, BP:180/110 mmHg, radial weak, carotid weak tender, femoral present. Epigastric and right flank bruit. Other systems were unremarkable.

Urine: Protein absent, no RBCs or WBCs.

Other evaluations:

• BUN- 8 mg/dl, serum creatinine- 0.6 mg/dl, Hb- 10 g/dl, S. Na- 139 meq/l, K- 3.5 meq/l
• USG- Right kidney was 7.5 cm and left kidney was 11 cm
• CMD maintained, no scarring- normal PCS

Analysis

Does the patient have kidney disease? Yes

What is the kidney disease? Renovascular hypertension or renal artery stenosis

What is the aetiology? Aortoarteritis; renal function normal

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Case 5

A male patient, 10 years old was referred for oligouria and increasing serum creatinine. Ten days prior, the child had fever which was treated as malaria. 

Physical examination: Decreased urine output, oedema of the feet, breathlessness on exertion, P- 110/min, BP- 140/100 mmHg, mild jaundice, mild oedema of the feet, RS- bilateral equal air entry, CVS- ejection, systolic murmur in left 2nd space. PA- no hepatic- spleenomegaly or acsitis; no focal neurological deficit.

Urine: Protein +, sugar absent, RBCs 8-10/hpf.

Other evaluations: CBC revealed Hb- 6 g/dl, Hct- 20%, TWBC- 12000/cmm, platelet count- 30,000/cmm, reticulocyte count- 15%, LDH- 2000, heptoglobulin- not detected, BUN- 70 mg/dl, serum creatinine- 7 mg/dl, S. Na- 132 meq/l, K- 5.8 meq/l, HCO3: 18 meq/l, C3- 50 (low) C4 normal.

Analysis

Does the patient have kidney disease? Yes

Where is the site of the lesion? Microvascular disease

What is the aetiology? TMA- Complement mediated HUS, most likely complement factor H antibodies

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Case 6

A female, 37 years old presents with weakness in all 4 limbs (sudden onset), no sensory symptoms, no bowel or bladder involvement, no history suggestive of cranial nerve paralysis, no diplopia, dysphagia.

Physical examination:

• Pulse- 110/min
• BP- 130/80 mmHg
• Mild thyroid enlargement
• No tremors
• No cranial nerve palsy
• Power in all 4 limbs- 1 to 2, reflexes absent, plantar flexor, no sensory deficit
• Other systems were unremarkable

Urine: Protein absent, No WBCs or RBCs. Urine pH was 6.5.

Other evaluations:

• CBC revealed Hb-13 g/dL, TWBC- 9000/cm, platelet- 320000/cm, BUN- 8 mg/dL, serum creatinine- 0.7 mg/dl, S.Na- 142 meq/l, K- 1.8 meq/l, CL- 110, HCO3- 20 meq/l, pH- 7.228, PCO2- 22.5
• PAO2- 92.8, HCO3- 18, O2-SAT 88.1%
• TSH- 100 µU/ml, TPO antibody positive

Analysis

Does the patient have kidney disease? Yes

Where is the site of lesion? Patient had hypokalemia muscle paralysis; cause of hypokalemia is distal renal tubular acidosis; aetiology- auto immune tubulitis.

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To read the previous article in this series, click here.

In the next part, Dr. NK Hase will answer questions posted by you on kidney disease.

Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.

The author Dr. NK Hase is a Director clinical Nephrology & Transplant working at Jupiter Hospital, Thane and former Professor & Head of Department of Nephrology Seth GS Medical College and KEM Hospital, Mumbai.