Year : 2019 | Volume
: 30 | Issue : 5 | Page : 1166--1170
A case of advanced chronic kidney disease with severe hypocalcemia, how to safely manage and dialyze?
Turki Al-Shebani, Mubashar Azeem, Elwaleed A Elhassan
Division of Nephrology and Renal Transplantation, King Abdulaziz Medical City, Riyadh, Kingdom of Saudi Arabia
Elwaleed A Elhassan
Division of Nephrology and Renal Transplantation, King Abdulaziz Medical City, P. O. Box 22490, Mail Code 1443, Riyadh 11426
Kingdom of Saudi Arabia
Patients often present with advanced chronic kidney disease (CKD) complicated with severe hypocalcemia that may be accompanied by electrocardiographic changes. The management of this kind of patients may require hemodialysis (HD). However, initiation of renal replacement therapy in this scenario needs special attention to avoid complications such as cardiac arrhythmias. A 22-year-old male presented to our emergency department with severe renal failure, hypocalcemia, hyperphosphatemia, severe acidosis, and QT prolongation on electrocardiography. The patient was kept in the emergency department under cardiac monitoring. He was started on IV calcium gluconate 1 g every 6 h aiming to increase his adjusted calcium level to 1.8 mmol/L. He subsequently received the first HD session with low blood flow, increased calcium, and decreased bicarbonate dialysate bath. There were no arrhythmias or hemodynamic instability. Intravenous calcium was discontinued; adjusted calcium improved progressively after dialysis and reached 1.9 mmol/L by the time of discharge and after receiving three sessions of HD. This case describes a not so infrequent presentation of advanced renal impairment with profound hypocalcemia, hyperphosphatemia in the setting of CKD-associated mineral bone disorder. Intravenous calcium administration may promote vascular and metastatic calcification, particularly with the coexistence of hyperphosphatemia, and hence, it is best avoided. There are no guidelines to direct initiating HD in this context. However, it appears that using a high calcium bath is prudent to minimize cardiovascular complications, particularly if there is the prolongation of the corrected QT interval on electrocardiography.
|How to cite this article:|
Al-Shebani T, Azeem M, Elhassan EA. A case of advanced chronic kidney disease with severe hypocalcemia, how to safely manage and dialyze?.Saudi J Kidney Dis Transpl 2019;30:1166-1170
|How to cite this URL:|
Al-Shebani T, Azeem M, Elhassan EA. A case of advanced chronic kidney disease with severe hypocalcemia, how to safely manage and dialyze?. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2021 Jun 16 ];30:1166-1170
Available from: https://www.sjkdt.org/text.asp?2019/30/5/1166/270275
Patients often present with advanced chronic kidney disease (CKD) complicated with severe hypocalcemia that may be accompanied by electrocardiographic changes. The management of this kind of patients may necessitate hemodialysis (HD). However, the initiation of renal replacement therapy in this scenario needs utmost attention to avoid possible cardiac arrhythmias. We describe a 22-year-old male who presented to our emergency department with severe renal failure, hypocalcemia, hyper-phosphatemia, acidosis, and QT prolongation on electrocardiography. The patient was kept in the emergency department under cardiac monitoring. After initial correction of hypo-calcemia with IV calcium gluconate, he was subsequently started on HD. After receiving three sessions of HD, he was well enough to be discharged.
Informed consent was obtained from the patient before presenting the report.
A 22-year-old male patient presented to our emergency department with complaints of shortness of breath associated with dizziness and fatigue for a few days’ duration. His past medical history was only notable for transient hematuria during childhood. He has not had any recent medical evaluation and is not known to be hypertensive or diabetic. He was not taking any medication. His family history was negative for kidney or cardiac diseases. He is single and unemployed.
On physical examination, he had a blood pressure of 180/113 mm Hg. His heart and respiratory rates were 90 and 17 breaths/min, respectively. His oxygen saturation on room air was 95% and he was afebrile. His weight was 63 kg with a body mass index of 21 kg/m2. He looked pale but was otherwise alert and in no apparent distress. His chest auscultation revealed bilateral basal crackles. The rest of his examination was unremarkable. Specifically, he did not exhibit Chvostek or Trousseau’s signs.
Investigations showed a urinalysis with protein of 300 mg/dL on dipstick. Arterial blood gas showed a pH 7.28, pCO2 39.2 mm Hg, and HCO3 of 18.1 mmol/L. Serum chemistries showed Na 140 mmol/L, K 5.6 mmol/L, Cl 103 mmol/L, total carbon dioxide 14 mmol/L, anion gap 23, blood urea nitrogen 39.6 mmol/L (110.9 mg/dL), creatinine 1525 mmol/L (17 mg/dL), albumin 36 g/L, total calcium 1.22 mmol/L, with an adjusted calcium 1.3 mmol/L (5.2 mg/dL) [according to the formula: adjusted calcium = serum calcium + 0.02 * (normal albumin – patient albumin)], PO4 2.5 mmol/L (7.7 mg/dL) with a calciumphosphate product of 3.25, Mg 0.64 mmol/L (1.26 mg/dL) and intact parathyroid hormone of 155 pml/L (1478 pg/mL). Ionized calcium was not available at our hospital. Hemoglobin was 99 g/L, with normal total white blood cell and platelet counts.
Initial electrocardiogram showed sinus rhythm at 79 beats/min with voltage criteria for left ventricular hypertrophy and nonspecific T-wave abnormalities. PR interval was 128 ms; QRS duration 70 ms; QT interval of 464 ms; corrected QT interval of 532 ms.
A chest radiograph showed interstitial and alveolar edema findings compatible with fluid overload. A renal sonographic scan demonstrated small kidneys (right measuring 7 cm and left 6.5 cm lengths). Both kidneys were shrunken and echogenic.
The patient was kept in the emergency department and kept under cardiac monitoring. He was given boluses of intravenous loop diuretics. He remained breathless despite diuretics, and thus, we decided to proceed with HD initiation for effective ultrafiltration. An emergent temporary dialysis catheter was inserted 15 h from arrival. For the hypocalcernia, he was begun on IV calcium gluconate 1 g every 6 h aiming to increase his adjusted calcium level to 1.8 mmol/L. He subsequently received the first HD session with the following prescription: blood flow rate 150 mL/min, dialysate of 200 mL/min, low-flux polysulfone dialyzer (F 6 HPS), and dialysate composition: (Na 135, K 2, Ca 1.75, HCO3 зо mmol/L). There were no arrhythmia or hemodynamic instability. Intravenous calcium was discontinued, and adjusted calcium improved progressively after dialysis and reached 1.9 mmol/L by the time of discharge after receiving three sessions of HD.
This scenario is not uncommon in our clinical practice. It reflects a late presentation of endstage renal disease with lost opportunities for early diagnosis and possible specific therapeutic interventions. Given his acid-base and electrolytes patterns, the following questions arose regarding initial management and crafting his dialysis prescription: (a) should the severe hypocalcemia be initially treated with intravenous or oral calcium or by neither? (b) should therapy be guided by the electrocardio-graphic features? (c) what are the best dia-lysáte calcium and base concentrations to use?
Hypocalcemia, which can be severe in CKD, is a consequence of diminished renal production of 1, 25-dihydroxyvitamin D and hyper-phosphatemia. Hyperphosphatemia results from low glomerular filtration of phosphate resulting in phosphate retention.
Calcium is approximately 40% bound to albumin and 45% circulating as physiologically active ionized calcium that is tightly regulated by parathyroid hormone (PTH) and Vitamin D. Moreover, ionized calcium level is affected by hyperphosphatemia and acid-base status. Low ionized calcium is a recognized cause of prolongation of QT interval and is well known to induce ventricular arrhythmias. Magnesium depletion can also cause hypocalcemia by creating PTH resistance that may occur when serum magnesium concentration falls <0.4 mmol/L (1 mg/dL), or by decreasing PTH secretion, which may be seen in patients with more severe hypomagnesemia.
The symptoms of hypocalcemia depend on the rate of its development and severity. The most common manifestations, in addition to fatigue and muscular weakness, are increased irritability, loss of memory, confusion, hallucination, paranoia, and depression. Clinical signs that may be elicited are Chvostek sign (contraction of the ipsilateral facial muscles elicited by tapping the facial nerve anterior to the ear) and Trousseau’s signs (induction of carpopedal spasm by inflation of a blood pressure pump above the systolic blood pressure for 3 min).
Corrected QT interval prolongation (QTc interval >440 ms in men or >460 milliseconds in women) represents a common ECG finding both among subjects from the general population and CKD patients. Data from the cardiovascular health study suggest that subjects with CKD not yet receiving dialysis exhibit longer corrected QT intervals compared with peers without CKD (estimated glomerular filtration rate, eGFR, >60 mL/min 1.73 m2). Considering that QT represents a measure of the cardiac repolarization time, an abnormally prolonged QT interval reflects a cardiac repo-larization defect and hence a greater vulnerability to left ventricular arrhythmias (i.e., torsade de pointes and ventricular fibrillation) and sudden cardiac death. Hypocalcemia is a recognized cause of prolongation of QT interval and is well known to induce torsade de pointes. A 76-year-old man with acute on chronic renal failure and hypocalcemia who was treated with ciprofloxacin for urinary tract infection developed prolonged QT interval complicated by torsade de pointes upon initiation of HD. It was presumed that the development of torsade de pointes compoundded multiple risk factors for prolongation of QT interval that include hypocalcemia and ciprofloxacin on a background of acute renal failure and acute worsening of metabolic disturbances at initiation of HD. The QT prolongation was corrected by treating the hypocalcemia. Hypocalcemia and ciprofloxacin are known to independently cause prolonged QT interval and torsade de pointes. The case illustrates that dialysis can trigger torsade on a background of this risk factor combination.
Regarding our patient, the absence of high-quality medical evidence precludes providing specific treatment recommendations. However, intravenous calcium administration should be avoided in the absence of symptoms or signs of hypocalcemia and especially with the COexistence of hyperphosphatemia. Calcium can precipitate with phosphorus and promote metastatic calcification. However, oral calcium salts in the form of carbonate or acetate can be used. Current 2017 KDIGO guidelines suggest that noncalcium-containing binders be generally used, except in situations where they are not available or affordable, or in such states like our patient who had severe hypocalcemia. Our patient underwent therapy with IV calcium gluconate, then begun on dialysis the following day. He did not have any arrhythmia and remained hemodynamically stable. On day 5, and after near normalization of serum calcium, he had a repeat electrocardiogram that showed persistently prolonged QTc but of less duration than the initial one (532 to 488 ms) raising doubt that it was solely caused by the severe hypocalcemia at presentation.
Ionized calcium is the physiologically active form, but is poorly correlated with total plasma calcium levels. If the ionized calcium cannot be obtained, the measured total plasma calcium level should be corrected to the serum albumin to verify the degree of hypocalcemia. Moreover, acid-base status can affect ionized serum calcium levels. Alkalemia increases the binding of calcium to albumin, thereby lowering the serum ionized calcium concentration. Chronic metabolic acidosis in patients with C KD causes an increase in ionized calcium due to less albumin binding that may not be captured by measurement of total calcium concentrations and thus helps protecting the patient from clinical manifestations of severe hypocalcemia.
Regarding dialysis prescription, it is generally recommended to use a dialysis bath with a calcium concentration of 1.5–1.75 mM (3.0–3.5 meq/L). The major concern in acute HD is that lower bath calcium concentrations may prolong and increase the variability of the QTc interval, both risk factors for sudden death. A study showed that QTc dispersion increased (potentially promoting arrhythmias) when a low calcium dialysis solution of (1.25 mM) was used. Serum calcium can also influence potassium-induced arrhythmias. Given how low the adjusted calcium was in our patient any calcium bath is expected to result in net influx of calcium during HD. Nevertheless, it might be prudent to use a higher calcium dialysis bath in patients with severe hypocalcernia, particularly if they have a pre-existing cardiac disease.
Alkalosis reduces the amount of calcium that exists in ionized form, and at least conceptually, correcting metabolic acidosis with dialysis can lower the ionized calcium concentration and exacerbate preexisting hypocalcernia. There are no randomized trials regarding the effect of different dialysate bicarbonate concentrations on hard outcomes. Literature suggests that the development of metabolic alkalosis after dialysis may contribute to adverse clinical outcomes., The main risk factors associated with high predialysis blood pH/serum bicarbonate leading to an increased risk of death in patients undergoing hemodialysis (HD) include hypercapnia, ionized hypocalcemia, hypokalemia, arrhythmias and prolongation of the QTc interval, hemodynamic instability, calcium phosphate precipitation and infection risk. For the present, target values for predialysis serum bicarbonate concentration have been established primarily based on observational studies and expert opinion. It has been suggested that dialysate bicarbonate concentration be individualized to keep predialysis serum bicarbonate level at least at 22 mmol/L. A patient new to dialysis with severe hypocalcemia will likely receive sufficient calcium from the dialysate to raise their serum ionized calcium level. A short and inefficient first session to prevent dialysis disequilibrium syndrome is unlikely to result in robust correction acidosis to an extent that impacts ionized calcium concentration.
In conclusion, this case describes a not so infrequent case of advanced renal impairment with profound hypocalcemia; hyperphosphatemia in the setting of CKD associated mineral bone disorder. There are no guidelines to direct initiating HD in this context. However, in the absence of symptomatic hypocalcemia, it appears that using only oral calcium salts, particularly if there is prolongation of the corrected QT interval on electrocardiography and using a high calcium bath, are prudent to minimize cardiovascular complications.
Conflict of interest: None declared.
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