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Approach to hyperkalemia

A case of type IV renal tubular acidosis

Lê Vĩnh Nghi, MD

Internal Medicine Resident

VinUniversity GME Program

The 24th National Scientific Congress of Vietnam Association of Critical Care Medicine, Emergency and Clinical Toxicology

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Renal physiology + Renal tubular acidosis

Normal tubules

Proximal: Absorb Bicarbonate (2)

Distal: Excrete Hydrogen (1)

Collecting: Aldosterone effect (4)

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RTA: CAN’T DO

Proximal: 2: Absorb Bicarbonate (HCO3-)

Distal: 1: Excrete Hydrogen (H+)

Collecting: 4: No Aldo or No Aldo effect → Hyperkalemia

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Pearls: Renal tubular acidosis

  • Non anion gap metabolic acidosis (NAGMA)

  • Undiagnosed (mostly)
  • Inherited forms < Acquired forms

  • Most common: type 4

Main cause: diabetic nephropathy → ↓renin ↓aldo

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Bello CHPRT et al. Diabetes mellitus and hyperkalemic renal tubular acidosis: case reports and literature review. J Bras Nefrol. 2017

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Case report: Clinical characteristic

74-year-old male, history: hypertension, type 2 diabetes mellitus, prior ischemic stroke, chronic kidney disease

Presents with hyperkalemia

For 6 months, he has been bedridden due to the stroke, eyes open, slow response, no talking. Nutrition through nasogastric catheter.

Monthly lab tests (CBC, CMP) at home

Meds: Valsartan, Amlodipine, Dapagliflozin, Rosuvastatin (long time)

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Case report: Clinical characteristic

History of present illness

Occasional lab test: K = 6.0. Turbid yellow urine 1200ml/day

No other symptoms (fever, nausea, vomiting, chest pain, shortness of breath, abdominal pain)

Physical examination: HR 80, BP 140/90, T 37, RR 15, W 50kg

Eyes open, slow response, no talking, not in pain distress, no edema

Normal heart and lung sounds, non-tender abdomen, no bladder distention, (R) weakness, turbid yellow urine on Foley catheter

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Labs results

Complete blood count, ECG: normal

  • Abdominal US: no kidney stone or tumor

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Comprehensive metabolic panel

Results

Glucose (mmol/L)

8.0

Urea (mmol/L)

9.5

Creatinine (umol/L)

140 (1.58 mg/dL)

eGFR (ml/min/1.73m2)

45

Na+ (mmol/L)

128

K+ (mmol/L)

6.0

Cl- (mmol/L)

100

Serum osmolality

273.5

pH

7.29

pCO2

23

HCO3- (mmol/L)

14

Lactate (mmol/L)

0.7

Anion gap

12 (normal)

Urine biochemistry

Results

pH

5.0

Leucocyte

500

Blood

(-)

Glucose

(-)

Albumin (mg/L)

80

Na+ (mmol/L)

60

K+ (mmol/L)

14.51

Cl- (mmol/L)

55

Creatinine (mmol/L)

2.076

Estimated urine osmolality (mmol/kg)

350

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Labs interpretation

Non anion gap metabolic acidosis (NAGMA)

Hyperkalemia

Suspected bacteruria

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K+ homeostasis: Do the kidneys work well ?

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Urine K excretion measurement

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TTKG

2 (< 7)

14.51 * 273.5

350 * 6.0

=

TTKG: low K excretion, suggesting hypoaldosteronism

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Hyperkalemia: Subsequent lab results

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Serum biochemistry (lying flat)

Results

Aldosterone (pg/mL)

7.0 (low) (12.0 – 157.50)

Renin (uIU/mL)

2.0 (low) (2.8 – 39.9)

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Hyperkalemia approach

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Non anion gap metabolic acidosis approach

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First Aid for the USMLE Step 2 CK 10e: Renal

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Renal tubular acidosis: Treatment

Correction of chronic acidemia

  • Type 1 + 2: Oral bicarbonate (dose 2 > dose 1) + Potassium
  • Type 4: ↓potassium, diuretics

Type 1: Acid secretion impairment, treat with Alkali

Type 2: Bicarbonate wasting, treat with Base (alkali)

Type 4: ALDOsterone disorder, treat with 4semide

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Patient’s treatment & progression

The patient was treated with potassium-lowering regimen:

Insulin – Glucose – Bicarbonate – Kayexalate – Furosemide

After, serum K+ 3,7 – 4.5, fully responded metabolic acidosis

→ Serum K+ responded to Furosemide therapy

Discharge after a week

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Renal tubular acidosis: Summary

  • Non anion gap metabolic acidosis (NAGMA)
  • Most common: type 4, main cause: diabetic nephropathy
  • Type 4: Hyperkalemia; Type 1 + 2: Hypokalemia

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Look for the cause

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