BRASH syndrome: the vicious cycle of bradycardia, hyperkalemia and renal failure

The increased success and availability of transplantation of solid organs other than kidneys has resulted in a large number of patients at risk for the usual medical complications of long-term immunosuppressive therapy. Acute and chronic renal failure play a critical role in the success of these

Renal artery stent revascularization with embolic protection in patients with ischemic nephropathy

Measuring urinary tubular biomarkers in type 2 diabetes does not add prognostic value beyond established risk factors

The aging kidney

BRASH SYNDROME: A DOWNWARD SPIRAL

Vasoconstrictor Therapy for the Hepatorenal Syndrome

Aim/hypothesis: The relationship between peripheral blood leukocyte telomere length (LTL) and kidney dysfunction, especially in people with hypertension, remains unclear. No clinical study has explored the role of inflammation and oxidative stress in the relationship between LTL and kidney dysfunction. Therefore, we examined the relationship between baseline LTL and albuminuria progression and/or rapid renal function decline in Chinese patients with or without hypertension and investigated whether inflammation and oxidative stress played a mediating role in this relationship. Methods: We conducted a prospective study including 262 patients in a 7-year follow-up period from 2014 to 2021. Data on LTL, inflammation, oxidative markers, renal function, and urine protein levels were assessed. Kidney dysfunction was defined as either albuminuria progression, rapid decline in renal function, or the composite endpoint (albuminuria progression and rapid decline in renal function). Logistic regression and simple mediation models were used for the analysis. Results: In this cohort (mean age, 54.3±9.7 years; follow-up period, 5.9±1.1 years), 42(16.0%), 21(8.0%), and 59(22.5%) patients developed albuminuria progression, rapid eGFR decline, and the composite endpoint of kidney dysfunction, respectively. Logistic regression analysis showed that each standard deviation decrease of baseline LTL and the lower quartile (Q) of baseline LTL were significantly correlated with an increased risk of rapid decline in renal function (OR=1.83 [95% CI 1.07, 3.27] per 1SD, P=0.03; OR=7.57 [95% CI 1.25, 145.88] for Q1 vs. Q4, P for trend=0.031); and the composite endpoint of kidney dysfunction (OR=1.37 [95% CI 0.97, 1.96] per 1SD, borderline positive P=0.072; OR=2.96[95% CI 1.15, 8.2] for Q1 vs. Q4, P for trend=0.036). The mediating analysis showed that tumor necrosis factor (TNF)-a partly mediated the relationship between LTL and rapid decline in renal function (direct effect: β=0.046 95%CI [0.006, 0.090],P=0.02; indirect effect: β=0.013 95%CI [0.003, 0.020]), and the mediating proportion was 22.4%.In subgroup analyses, LTL was inversely associated with rapid decline in renal function or the composite endpoint of kidney dysfunction only in patients with hypertension (OR=49.07[3.72,211.12] vs.1.32[0.69,2.58] per 1SD, P for interaction=0.045;OR=3.10 [1.48, 7.52] vs.1.08[0.92,1.63] per 1SD, P for interaction=0.036). Conclusion: Baseline LTL could independently predict kidney dysfunction at follow-up, especially in participants with hypertension. TNF-a partially mediated the negative association between LTL and kidney dysfunction.

We examined the association between home and office blood pressure (BP) levels and further decline in renal function among treated hypertensive patients with and without renal dysfunction. We calculated annual decline in estimated glomerular filtration rate (ΔeGFR) in 1535 treated hypertensive patients with home and office BP measurements. We defined ΔeGFR <0 as decline in renal function, and ΔeGFR ⩾0 as non-decline in renal function based on 1.5 years of follow-up. For 520 patients with low eGFR at baseline, morning home, evening home and office systolic BP (SBP) levels and morning home diastolic BP (DBP) levels were positively associated with the risk of decline in renal function (trend P=0.003, 0.002, 0.003 and 0.004). Compared to patients with home SBP <125 mm Hg, the risk of decline in renal function was higher in those with home SBPs ⩾135 mm Hg and between 130-135 mm Hg, while the risk was similar in those with home SBP of 125-130 mm Hg. For 1015 patients with normal eGFR at baseline, only morning home SBP level was positively associated with the risk of decline in renal function (trend P=0.004). Morning home BP might be useful for risk evaluation of decline in renal function even among treated hypertensive patients with normal renal function. Target levels of home BP control among treated hypertensive patients need to be further investigated.

Background and Aims Oxalate nephropathy is a rare cause of renal failure which is usually due to primary or secondary hyperoxaluria. Secondary hyperoxaluria results from increased intake or increased intestinal oxalate availability (enteric hyperoxaluria), increased intestinal oxalate degradation, or increased colonic permeability to oxalate [1]. Little is known about the burden of end stage kidney disease in this group of patients as most of the initial literature was from case reports and case series. More recently, prevalence of 1- 4.01% was reported from biopsy studies suggesting that this entity is indeed a cause of kidney failure that needs to be considered [2,3]. Method We present two cases of oxalate nephropathy secondary to enteric hyperoxaluria following small bowel resections. Results CASE ONE 82 year old man with a solitary kidney who was admitted in the ED on account of a decline in renal function on a background of episodes of loose stools. This was his second admission in two months on account of decline in renal function. He had emergency laparotomy and adhesiolysis as a result small bowel obstruction from volvulus 12 months earlier. Other past medical history include left nephroureterectomy for renal cancer, transurethral resection of bladder tumour, hypertension, Barretts and appendectomy. His medications were Omeprazole(which was switched to Famotidine due to hypomagnesaemia 7 months postop), Atenolol and Adcal D3. Renal immunology and myeloma screen were negative. Urine was bland and ultrasound did not show any obstruction. His AKI was initially thought to be pre-renal and there was some improvement in renal function with fluids during his first admission although renal function didn't return to baseline. His renal function progressively worsened in a spate of a few months. He had a baseline creatinine of 130 prior to his laparotomy which worsened to 184 post surgery bur the improved to about 109 few days post op. However, his renal function was noticed to decline 9 months post op and eventually his creatinine peaked at 751, fourteen months post op. He eventually had a renal biopsy 13 months post op that showed oxalosis, acute tubular injury and patchy interstitial fibrosis. His renal function continued to deteriorate and he was eventually commenced on haemodialysis. CASE TWO A 75-year-old man who was referred to the renal clinic on account of a decline in renal function. He had a past medical history of Crohn's disease, previous right hemicolectomy 26 years ago with revision 4 years ago, ileostomy(with subsequent reversal), inguinal herniorrhaphy, hypertension and BPH. He was on Azathioprine for his Crohn's and his initial decline in renal function was thought to be attributable to Azathioprine. Other medications include: Amlodipine 5 mg, Finasteride 5 mg, Loperamide 2 mg bd, Tamsulosin 400mcg od. At referral, his renal function had progressively deteriorated over the previous few months from a baseline creatinine of 145 to 303, 44 months after his last surgery. Urinalysis showed trace of protein and + of blood however, urine ACR was normal. Vasculitis and myeloma screen were also normal. Ultrasound ruled out any obstruction. Despite pausing Azathioprine, renal function continued to deteriorate with creatinine peaking at 561 over the next 2 months. He subsequently had a renal biopsy that showed chronic damage with oxalate casts. He was subsequently commenced on haemodialysis. Conclusion These two cases highlight the need to consider enteric hyperoxaluria in patients presenting with unexplained decline in renal function who have had bowel surgery or have risk factors for fat malabsorption. This is important due to the usual poor prognosis in this group of patients [1].

ObjectivesTo establish the effect of pregnancy on deterioration of renal function in women with Chronic Kidney Disease (CKD) stages 3–5 attending the renal antenatal clinic.MethodsAll women with excretory renal dysfunction...

Primary Versus Secondary Prevention of Chronic Kidney Disease: The Case of Dietary Protein

Smoking is a risk factor in the progression to kidney failure

Impairment of renal function is common among elderly patients due to an age-related decline in renal excretory function. In addition, many diseases such as hypertension and diabetes mellitus are associated with an accelerated decline in renal function. Renal dysfunction affects the metabolism of compounds and thus has important therapeutic consequences for drug safety. For pain patients who have reduced renal function such as those in palliative care, most opioids used for chronic pain treatment should be administered at reduced dosages, with increased dosage intervals, or not at all because of the risk of accumulation of the parent compound or its metabolites. For instance, for morphine or codeine, active metabolites are formed in the liver and cleared by the kidney and may therefore accumulate in cases of renal dysfunction. In contrast, buprenorphine can be administered at normal doses in patients with renal dysfunction because it is mainly excreted through the liver. In patients undergoing regular haemodialysis treatment, removal of an opioid during dialysis varies between individuals based upon a number of factors including the dialysis technique used. Morphine appears to be difficult to process in haemodialysis patients due to possible ‘rebound’ of metabolites between dialysis sessions. By contrast, the pharmacokinetics of buprenorphine are unchanged in haemodialysis patients, which means that there is no need for dose-reduction with this drug. Thus, in patients with reduced renal function, chronic renal insufficiency and haemodialysis, buprenorphine appears to be a safe choice when opioid treatment is initiated.

Left Ventricular Assist Devices and Renal Ramifications.

Decline in Renal Function after Partial Nephrectomy: Etiology and Prevention