BackgroundParathyroidectomy (PTX) is done in cases of secondary hyperparathyroidism from chronic kidney disease to improve renal osteodystrophy. Despite this widespread practice, clinical outcomes regarding the benefits of this procedure are still lacking. Most studies in the literature have opted to report the laboratory outcome instead. Our study aimed to evaluate the postoperative clinical course for patients who had undergone total PTX without autoimplantation.Methods and resultsAll patients who underwent PTX between January 2010 and February 2014 in a tertiary referral center were included in this study and followed up for 12 months. Laboratory outcome parameters include various preoperative and postoperative serial measurements of laboratory parameters. Patients’ hospitalizations and mortality records post-PTX were also retrieved and recorded. In all, 90 patients were included in this study. The mean age was 48 ± 18 years. The majority of the patients (54.4%) were male and 90% were on hemodialysis. The mean duration of dialysis was 8.0 ± 5.0 years. Indications for PTX were symptomatic bone pain (95.6%), fractures (3.3%) and calciphylaxis (1.1%). Mean preoperative values for serum calcium, phosphate, alkaline phosphatase and intact parathyroid hormone (iPTH) were 2.40 ± 0.23mmol/L, 1.92 ± 0.51 mmol/L, 689.60 ± 708.50 U/L and 311.90 ± 171.94 pmol/L, respectively. The majority (92.2%) had all four glands removed and 92.2% of the glands showed hyperplasic changes. One year after PTX, 90 patients (100%) had serum iPTH <8 pmol/L and 28 patients (31%) had unmeasurable iPTH levels. A total of 15% of patients had hospitalizations for various reasons and of these, 50% were within 90 days. The mean hospital stay was 14.4 ± 18.6 days. The mortality rate was 4.4% and of these, 25% were in first 30 days. Causes of death were mainly from sepsis (75%) and acute coronary syndrome (25%). One patient (1.1%) had a relapse.ConclusionsEven though PTX markedly reduces postoperative serum iPTH levels, it carries with it significant risk of morbidity and mortality.
BackgroundAlthough there is a large volume of literature regarding the definition and epidemiology of.Type 2 diabetes nephropathy (T2DN). There has been a paucity of data focused on the rate of transition of T2 DN. Based on our personal observation a certain percentage of our incident end stage renal disease (ESRD) patients from T2DN experienced a rapid decline of renal function. Their rapid decline nature of glomerular filtration rate (GFR) of 46 to 60 mL/min per 1.73m2 per year have far exceeded the KDIGO definitions of acute kidney injury (abrupt decrease in kidney function occurring over 7 days or less), acute kidney disease (acute or subacute damage and/or loss of kidney function for a duration of between 7 and 90 days after exposure to an acute kidney injury initiating event (Chawla et al Nat Rev Nephrol 241–57 2017) or even rapid decliner (eGFR declines > 5 mL/min per 1.73m2 per year) (Chawla et al Nat Rev Nephrol 241–57 2017; Andrassy Kidney Int 622–623 2013).Case presentationWe describe here three cases of type 2 diabetic patients that have rapid renal deterioration with rate of decline 46 - 60 mL/min per 1.73m2 per year. All the patients are heavily nephrotic. All of the renal biopsies done showed the classical diabetic changes, hypertensive changes, diffuse tubulointerstitial damage, and interstitial nephritis. All of the patients admitted to taking various form of traditional medications in hope of curing their renal disease.ConclusionWe wish to highlight that type 2 diabetics with massive nephrotic range proteinuria have enhanced risk of rapid renal function deterioration. The patients should be educated about the risks of rapid renal function deterioration when there is presence of heavy proteinuria. High grade proteinuria is likely to inflict the diffuse tubulointerstitial inflammation. The interstitial nephritis could be further worsened by traditional supplements consumption. Timely health education and advice must be undertaken to retard this unwanted rapid renal disease progression.
Category: RRT ResearchPresenter: Dr FARIZ SAFHAN MOHAMAD NOR Keywords: vancomycin, continuous renal replacement therapy, pharmacokinetic Introduction: Achieving optimal vancomycin dosing, particularly in septic critically ill patients receiving continuous renal replacement therapy (CRRT) is crucial. Established guidelines recommend the use of trough concentrations to manage vancomycin dosing in adult patients with gram-positive infections. Importantly, obtaining the area under the plasma concentration-time curve (AUC), based on the pharmacokinetic / pharmacodynamics (PK/PD) concept, is extremely required.Objective: This study aimed to describe the pharmacokinetics (PK) of vancomycin in Malaysian critically ill patients receiving CRRT, and the achievement of its therapeutic target, the ratio of the AUC to the minimum inhibitory concentration (MIC) of causative pathogen (AUC/ MIC >400), using a standard dosing regimen (750 mg 12 hourly). Methodology: This was a prospective PK study of vancomycin using standard dosing regimen, in critically ill patients receiving continuous venovenous haemofiltration (CVVH). Blood samples were collected at ten sampling times during a dosing interval. PK analyses were evaluated using non-compartmental method. Vancomycin trough concentrations (15-20 mg/L), and the achievement of the ratio of AUC/ MIC>400, based on selected susceptibility breakpoint (MIC¼1 mg/L), were evaluated. Results: Fifty blood samples from five PK profiles of five patients were analysed. The median (interquartile range) of vancomycin total clearance (CL total ) and volume of distribution (V d ) were 62.8 (45.1-62.7) mL/ min and 62.0 (48.7-94.2) L respectively, during CVVH. Maximum concentration, C max [30.8 (30.5-33.2) mg/L] was observed at 1.8AE0.3 h. The standard dosing regimen (750 mg 12 hourly) resulted in AUC 0-24 and C min of 400.1 (399.0-504.1) mg.h/L and 12.1 (10.7-16.1) mg/L, respectively. Of these, only two patients, who were anuric, obtained trough concentration between 15-20 mg/L and subsequently achieved the targeted AUC/MIC>400 (MIC¼1 mg/L).
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