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- Department of Pathology, Hamad Medical Corporation, Doha, Qatar [1]
- Division of Nephrology, Department of Medicine, Hamad Medical Corporation, Doha, Qatar [1]
- Hamad General Hospital, Hamad Medical Corporation, Qatar. Email and ORCID ID: [email protected] & https://orcid.org/0000-0002-7289-4942 [1]
- MICU, Hamad Medical Corporation, Doha, Qatar [1]
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High-dose potassium resuscitation in a peritoneal dialysis patient with severe hypokalemia and torsades de pointes
Background: The American Heart Association (AHA) recommends to treat cardiac arrest due to Torsade de Pointes (TdP) with 1–2 grams of intravenous (IV) magnesium over 5 minutes. A second dose can be repeated within 5–15 minutes and a continuous infusion may be considered. In cases of TdP due to severe hypokalemia the doses and rate of administration of IV potassium chloride (KCL) are not described explicitly in the guidelines.
Methods: In this case report we describe a peritoneal dialysis (PD) patient who had a prolonged history of hospital stay with infected diabetic foot. He was on the medical ward but recently admitted to the Intensive Care Unit with septic shock needing inotropic support. He developed a TdP cardiac arrest with a serum potassium of 2.4 millimol/litre. We managed the cardiac arrest according to AHA guidelines and also administered a total of 120 milliEquivalent (mEq) of KCL over 2 hours. The severe refractory hypokalemia improved and the recurrent TdP subsequently stopped only after we urgently drained the PD fluid during the resuscitation as a last resort. We also avoided administration of sodium bicarbonate even though he was severely acidotic during and after the resuscitation.
Results: To compliment this case report we reviewed the literature available on hypokalemia in PD patient and also on the established treatment of TdP.
Conclusion: In cardiac arrest situation secondary to hypokalemia repeated high doses of IV KCL up to a total of 120 mEq may be required provided point of care testing is available. Draining the PD fluid during resuscitation might expedite the correction of the refractory hypokalemia and malignant arrhythmias.
Atypical Anti-Glomerular Basement Membrane Disease With Diffuse Crescentic Membranoproliferative Glomerulonephritis: Case Report and Review of Literature
Anti-glomerular basement membrane (anti-GBM) disease occurs in fewer than two cases per million population. Patients usually present with features of rapidly progressive glomerulonephritis (RPGN) with or without pulmonary involvement. Anti-GBM disease is classically diagnosed by both demonstrating GBM linear immunofluorescence staining on kidney biopsy and detecting anti-GBM antibodies in serum. More than 90% of patients with anti-GBM disease either become dialysis-dependent or die if left untreated.
Here we report a 37-year-old man who presented with bilateral lower limb edema hypertension acute kidney injury (creatinine of 212 μmol/L) microscopic hematuria and nephrotic range proteinuria (15 g/day). His kidney biopsy showed diffuse crescentic membranoproliferative glomerulonephritis and bright linear staining of GBM by immunoglobulin G consistent with anti-GBM disease; however serum anti-GBM antibodies were negative. The patient was diagnosed with atypical anti-GBM disease and treated aggressively with intravenous pulse steroids plasmapheresis oral cyclophosphamide and oral prednisolone with significant improvement in kidney function and proteinuria.
Atypical anti-GBM disease should be considered in patients presenting with RPGN even in the absence of serum anti-GBM antibodies. Early diagnosis and aggressive treatment in such cases are warranted to prevent irreversible kidney damage as the course of the disease might not be as benign as previously thought.
Risk factors associated with chronic kidney disease progression: Long-term retrospective analysis from Qatar
Introduction: The risk factors influencing the natural course of chronic kidney disease (CKD) are complex and heterogeneous. Recognizing the factors associated with CKD progression can enable the identification of high-risk patients for more intensive treatment.
Patients and methods: A retrospective evaluation of CKD patients was performed under follow-up between January 1 2001 and December 31 2016 at a tertiary health care center.
Results: Among 5370 screened patients 1020 patients with complete data were included in the analysis. The median follow-up period for the studied patients was 9.3 years. Based on the analysis 120 (11.8%) patients had reached end-stage kidney disease “ESKD” or death. The study revealed that the risk factors associated with reaching ESKD and/or death using Kaplan–Meier survival curve and log rank test included higher hemoglobin A1c among diabetic patients higher grade of proteinuria and non use of renin-angiotensin system blockers. The patients with CKD progression constituted 77.2% of all CKD patients. The study findings indicated that older age Arab ethnicity smoking habit diabetes mellitus and hypertension (presumed as original kidney diseases) are among the significant risk factors associated with a further decline of the estimated glomerular filtration rate (eGFR) and further CKD progression.
Conclusion: This study summarized the demographic and clinical risk factors associated with CKD progression and patients’ outcomes among a unique and heterogeneous population in the state of Qatar. Intensive treatment of modifiable risk factors could be of value in halting the progression of CKD. However prospective studies are warranted to confirm our findings.