Acute life-threatening hyperkalaemia in a patient with giant hydronephrosis: a case report

Abstract

A 52-year-old man with a history of urolithiasis presents to the emergency department with a sudden, sharp, continuous right flank colicky pain. Laboratory workup demonstrates acute kidney injury with a mild hyperkalaemia. During the observation period, the patient develops an atypical broad complex sinus bradycardia and eventually short asystolic periods. This was caused by a severe therapy-resistant hyperkalaemia, wherefore emergency haemodialysis was necessary. Radiographic results showed a giant hydronephrosis with a blowout of the right kidney and an obstructing calculi of 21 mm in the distal ureter. We will discuss the mechanism of reversed intraperitoneal dialysis causing the refractory hyperkalaemia and the need of close ECG monitoring in patients where kidney blowout is considered.

Background

We report an interesting case of an acute life-threatening hyperkalaemia, caused by a blowout of the right kidney. In our patient, acute kidney injury developed within hours with a refractory hyperkalaemia and cardiac arrhythmias. It underlines the importance of close observation when a blowout is suspected, in particular continuous ECG monitoring.

Acute kidney injury, also known as acute kidney failure, is an acute loss of kidney function that occurs when the kidneys suddenly become unable to filter waste products from the blood. When this filtering ability is lost, dangerous levels of waste products and electrolytes, like potassium, may accumulate.

Severe hyperkalaemia is defined as a serum or plasma potassium level greater than 6.5–7.0 mmol/L. Most common causes of acute hyperkalaemia include acute tubular necrosis, digitalis toxicity, burn injuries, head trauma, hypocalcaemia, rhabdomyolysis, tumour lysis syndrome, metabolic acidosis and post renal kidney failure. Symptoms such as life-threatening cardiac arrhythmias, muscle weakness or paralysis usually develop at these higher levels, but the rate of change is more important than the numerical value.¹

These symptoms in combination with ECG abnormalities are cornerstones in determining the management of hyperkalaemia.

The toxic effects of hyperkalaemia on the cardiac conduction system are potentially lethal. Acute management is primarily done by stabilisation of the myocardial cell membrane with calcium salts and potassium-shifting agents, such as insulin/glucose and salbutamol. However, definitive therapy by means of dialysis, potassium-binding agents and loop diuretics is necessary to remove potassium from the body. Acute dialysis treatment is recommended in patients with acute kidney failure. In case of severe hyperkalaemia, continuous ECG monitoring and frequent re-evaluation of potassium concentrations are recommended to assess treatment effect and observe acute cardiac arrhythmias.²

The case

A 52-year-old man with a history of urolithiasis was admitted to the emergency department of our hospital with a sudden onset sharp continuous right flank colicky pain. The pain was not postprandial nor were there other triggers. On admission, his blood pressure was 127/84 mm Hg and his pulse was regular with a rate of 80 beats/min. He was not dyspnoeic and his abdomen was obese and non-tender, without any loin pain. Murphy’s test was negative.

The patient was a cigarette smoker who never used alcohol, with a history of coronary artery disease, hypertension, gout and urolithiasis. There was an unclear history of a previous giant kidney seen on ultrasound, without specialist follow-up. He did not experience loin pain related to his urolithiasis over the past 20 years. His regular medication was amlodipine, valsartan, allopurinol, metoprolol, simvastatin and acetylsalicylic acid. No allergies were known.

Investigations

Blood samples were taken from a newly placed peripheral venous catheter on admission (table 1).

Table 1.

Blood sample on admission

Test	Result T0	Result T4.5	Laboratory reference ranges in healthy adults
Haemoglobin	12.2		8.5–11.0 mmol/L
Hematocrit	0.59		0.40–0.50 mmol/L
Lactate dehydrogenase	339		<250 U/L
Alkaline phosphatase	145		40–120 U/L
gamma-glutamyl transferase	92		<55 U/L
Lipase	58		<60 U/L
Creatinine	229	435	60–110 µmol/L
Urea	10	16	2.5–6.4 mmol/L
Sodium	142	129	135–145 mmol/L
Potassium	5.1	8.0	3.5–5.0 mmol/L
C-reactive protein	11		<6.0 mg/L
White Blood Cell	15.7		4.0–10.0×109/L

T0: Results at admission time. T4.5: Results 4.5 hours after admission.

The acute kidney injury with a creatinine of 229 µmol/L and a leukocytosis of 15.7×10⁹/L were the most significant abnormalities.

His ECG on admission showed left axis deviation and a first degree AV block (Atrioventricular block) (figure 1). The radiologist performed an ultrasound of the kidneys. This showed a giant right kidney with free abdominal fluid. Additionally, an abdominal CT scan with intravenous contrast was performed directly and showed an atypical, multicystic right kidney of 27 cm with giant hydronephrosis and severe parenchymal loss. Significant retroperitoneal and intraperitoneal free fluid was seen, most likely caused by blowout of the right kidney (figure 2). Furthermore, an obstructing calculi of 21 mm was seen in the right distal ureter. A previous ultrasound report from another hospital in 2007 (13 years before presentation) already described a multicystic kidney, measuring 19 cm. There were no signs of hydronephrosis. No follow-up plan was made.

Figure 1.

ECGs. (A) ECG on admission. (B) Repeat ECG, broad complex rhythm 75/min. (C) Repeat ECG, broad complex sinus rhythm 45/min. (D) Repeat ECG, progressive broad complex sinus rhythm with an asystole episode. (E) Repeat ECG after emergency haemodialysis, normalised ECG.

Figure 2.

CT scan images. (A) Initial scan with atypically enlarged kidney of 27 cm. (B) CT scan after 6 months.

Clinical course

Shortly after the CT scan, the patient developed a short lasting tachycardia of 150 bpm on continuous monitoring without any change of his clinical appearance or blood pressure. A repeated ECG showed an atypical broad complex sinus rhythm of 75 bpm (figure 1). A venous blood gas was immediately performed, showing a metabolic acidosis with a hyperkalaemia of 7.8 mmol/L (table 2). This was measured 4.5 hours after the initial blood sample. During this, the creatinine level had risen from 229 to 435 µmol/L, and the ECG was evolving into a broad complex bradycardia with a rate of 45 bpm (table 1, figure 1).

Table 2.

Venous blood gas

Test	Results T4.5	Results T5.5	Laboratory reference ranges in healthy adults
pH	7.28	7.23	8.5–11.0 mmol/L
HCO3-	17.5	16.1	22.0–29.0 mmol/L
PCO2	38	42	32–45 mm Hg
Hb	11.5	10.9	8.5–11.0 mmol/L
Na	130	127	135–145 mmol/L
K+	7.8	7.9	3.5–5.0 mmol/L
Ca	1.11	1.15	1.10–1.30 mmol/L
Lactate	1.7	2.0	0.9–1.7 mmol/L

T4.5: 4.5 hours after admission. T5.5: 5.5 hours after admission.

According to our protocol, hyperkalaemia treatment was started with 10 mL bolus of calcium gluconate 20 units of 10% regular insulin intravenous in 50 mL of 50% glucose. The ECG did not improve, and the venous blood gas and regular potassium were repeated (arterial blood gas failed) 1 hour after the initial venous blood gas was taken. The gas showed a slightly progressive metabolic acidosis with a pH of 7.23 and a potassium of 7.9 mmol/L (table 2). Ten millilitres of calcium gluconate and 20 units of 10% regular insulin intravenous in 50 mL of 50% glucose were repeated and 100 cc 8.4% NaHCO3 was additionally given. Because of the refractory hyperkalaemia and progressive ECG abnormalities with short asystolic periods (figure 1), the patient was immediately transferred to the Intensive Care Unit for emergency haemodialysis. The potassium was decreased to 5.0 mmol/L after haemodialysis and the broad complex bradycardia normalised (figure 1).

Outcome and follow-up

The patient had an uneventful and uncomplicated follow-up period. After one dialysis treatment, kidney function resolved. Two days after initial presentation, a double J stent was placed and renal function improved (creatinine 113 µmol/L). After 4 days, the patient was discharged home. Ten days later, in a follow-up visit, he was doing well and had a normal functioning capacity. He had lost 14 kg and his abdomen had decreased in size.

Two months later, an ureterorenoscopy was performed, the renal calculi was removed and the double J stent was replaced and maintained for another 10 weeks. Renal function was measured with a dimercaptosuccinic acid (DMSA) scan and showed a barely visible right kidney with a function of 17%, compared with the healthy left kidney with a function of 83%. An additional ultrasound showed multiple organised fluid collections in the right kidney, most likely cysts. During the 6-month follow-up visit, an abdominal CT scan was performed and showed improvement of kidney abnormalities without other calculi and a small amount of normal parenchyma (figure 2). A nephrectomy was considered but because of the remaining stable kidney function at 6-month follow-up (creatinine 119 µmol/L) and the absence of symptoms and new stones, a conservative treatment was maintained. Close follow-up of kidney function and kidney size, using abdominal CT and ultrasound, was arranged.

Discussion

The ultrasound report from 2007 reported a big, multicystic right kidney without signs of hydronephrosis. Multiple cysts were still seen on the repeat ultrasound during the 6-month follow-up in our hospital. A simple kidney cyst is a pocket of fluid that originates from the surface of the kidney and is contained by a thin wall.³ A kidney with multiple cysts will have a more fragile renal cortex than a kidney without any cysts. This vulnerability may have contributed to the kidney blowout in our case.

Literature reports pelvic-ureteric junction obstruction as the most common cause of giant hydronephrosis, followed by stones in the upper ureter. Other less common causes include obstructive mega ureter, trauma, congenital ureteral narrowing, ureter pelvic tumours, renal ectopia, retroperitoneal fibrosis and ureteric atresia.⁴ Beside the obstructing calculi of 21 mm in the distal ureter, no other causes of hydronephrosis were found in our case.

The mechanism triggering the raise in creatinine and potassium levels in this case can be best explained by the renal blowout caused by the obstructing calculi. In normal circumstances, the body excretes about 100 µmol of creatinine per day.⁵ In case of acute and total kidney shutdown, serum creatinine usually rises about 100 μmol/day. Therefore, a physiological creatinine level raise of 200 µmol within a couple of hours is impossible. Based on the CT images, little urine production was expected from the kidney. Over time (hours to days), the concentration of creatinine and potassium in the renal pelvis will equilibrate to the same level as the serum, unless there is still a supply of fresh urine from an active kidney. The DMSA scan showed kidney function of 17%, which indicates active production of urine. The most accepted theory of the raise in creatinine and potassium levels, based on the initial symptoms of the patient and the radiographic imaging, is that of a rupture of the renal pelvis with leakage of fresh urine into the abdomen and retroperitoneum also known as reversed intraperitoneal dialysis. Urine is known to have high concentrations of creatinine and potassium and will be absorbed by the peritoneum.^{6 7} This intravascular absorption caused a rapid raise of serum creatinine levels and the acute and refractory hyperkalaemia, in turn, causing a life-threatening arrhythmia. There was no evidence of other causes of hyperkalaemia such as acute tubular necrosis, digitalis toxicity, severe acidosis, trauma, rhabdomyolysis, tumour lysis syndrome or post renal kidney failure.

Similar cases of acute creatinine raise and hyperkalaemia due to reabsorption of urine have been described in other case reports. In 2015, Matsumura et al described a case of hyperkalaemia and pseudo-renal failure after urinary ascites due to spontaneous bladder rupture following transurethral resection of a bladder tumour.⁸ In 2020, Simler et al reports an acute raise in creatinine and potassium after a traumatic bladder rupture.⁹

Conclusion

Our report presents an interesting case of an acute life-threatening hyperkalaemia and renal impairment, most likely caused by a blowout of the right kidney after obstruction by a stone. In this case, hyperkalaemia is caused by urine reabsorption by the peritoneum, also known as reversed intraperitoneal dialysis.

This rare event emphasises and supports the need of close ECG monitoring in patients where kidney blowout is expected, as in this case blowout caused therapy-resistant hyperkalaemia with cardiac arrhythmias. Therefore, clinicians should be aware of this risk, and close monitoring of heart rhythm, potassium and renal function is essential in similar cases.

Learning points.

• This case report supports the need of close ECG monitoring in patients where kidney blowout is expected, as in this case blowout caused therapy-resistant hyperkalaemia with arrhythmias.

• In some cases, a blowout can cause extreme hyperkalaemia which requires close ECG monitoring.

• In this case, hyperkalaemia is partly caused by the resorption of urine, also known as reversed intraperitoneal dialysis.

• First, this extreme hyperkalaemia has got to be treated by emergency haemodialysis, but for definite treatment, a double J stent needs to be placed to drain the hydronephrosis.