Background: The World Health organization (WHO) declared COVID-19 as a global pandemic in March of 2020. Many studies have assessed the association between different comorbidities and COVID-19 outcomes. In this overview of reviews, we aim to summarize the association between CKD and different COVID-19 outcomes. Methods: We performed a systematic search through Embase, PubMed, Epistemonikos, and Cochrane as well as preprint databases from January 1, 2020 to January 5, 2021. After searching systematic reviews, we updated the search by identifying primary studies published after August 2020, which was the date of last search in the reviews. We focused on systematic reviews and large primary studies. We followed the GRADE methodology to assess the certainty in effect estimates. Data was pooled based on random effects model. Results: We included a total of 69 systematic reviews and 66 primary studies in our overview. We did not identify any systematic reviews that directly reports on CKD and the risk of contracting COVID-19. There was no convincing difference on the risk of acquiring COVID-19 infection in patients with and without CKD in primary studies (OR = 1.00, 95% CI 0.76-1.33). CKD is associated with higher risk of COVID-19 related mortality pooled hazard ratio (HR) 1.48 (95% CI 1.33-1.65) and pooled odds ratio (OR) 1.77 (95% CI 1.54-2.02)(moderate certainty), hospitalization pooled risk ratio (RR) 1.63 (95% CI 1.03-2.58) (moderate certainty) and disease severity pooled RR 1.56 (95% CI 1.3-1.86) (moderate certainty). Notably, the risk of COVID-19 attributed hospitalization and mortality were higher in patients with more advanced CKD stage. Conclusions: Evidence consistently demonstrated an increased risk of mortality, hospitalization and disease severity in patients with CKD and COVID-19 infection. The results highlight the importance of recognizing patients with CKD as a high-risk group and of prioritizing these patients for COVID-19 prevention strategies including vaccination.
Abstract Background Malakoplakia is a rare granulomatous inflammatory condition that can affect immunosuppressed patients. The genitourinary system is the most involved organ. We present a case of kidney failure caused by obstructing bladder lesions, clinically suspicious for malignancy and pathologically proven to be malakoplakia. Case presentation A 70-year-old woman presented with acute kidney injury and Escherichia coli (E.coli) bacteremia. Investigation showed bilateral hydronephrosis with thickening of the renal pelvises suggestive of urothelial malignancy. Cystourethroscopy revealed multiple bladder lesions completely obliterating both ureteral orifices. Pathology of the resected lesions confirmed the diagnosis of malakoplakia. Patient was treated with a prolonged antibiotic course over 6 months with recovery of her kidney function. Conclusion Malakoplakia can mimic invasive tumors, and the diagnosis is only attained through histopathology which uniquely demonstrates the pathognomonic Michaelis–Gutmann inclusions inside sheets of histiocytes. Treatment is largely dependent on prolonged antibiotics therapy that must cover the most common isolated pathogen, E.coli.
Background: COVID-19 provided a real challenge for evidence synthesis due to the rapid growth of evidence. We aim to assess the impact of including all studies versus including larger studies only in systematic reviews when there is plethora of evidence. We use a case study of COVID-19 and chronic kidney disease (CKD).Methods: The review team conducted a systematic review of multiple databases. The review assessed the effect of CKD on mortality in patients with COVID-19. We performed a sensitivity analysis to assess the effect of study size on the robustness of the results based on cutoffs of 500, 1000 and 2000 patients.Results: We included 75 studies. Out of which there were 40 studies with a sample size of >2,000 patients, seven studies with 1,000-2,000 patients, 11 studies with 500-1,000 patients, and 17 studies with <500 patients. CKD increased the risk of mortality with a pooled hazard ratio (HR) 1.57 (95% confidence interval (CI) 1.42 - 1.73), odds ratio (OR) 1.86 (95%CI 1.64 - 2.11), and risk ratio (RR) 1.74 (95%CI 1.13 - 2.69). Across the three cutoffs, excluding the smaller studies resulted in no statistical significance difference in the results with an overlapping confidence interval.Conclusions: These findings suggested that, in prognosis reviews, it could be acceptable to limit meta-analyses to larger studies when there is abundance of evidence. Specific thresholds to determine which studies are considered large will depend on the context, clinical setting and number of studies and participants included in the review and meta-analysis.
Collagenofibrotic glomerulopathy (CG) also known as collagen type 3 glomerulopathy is a rare disease characterized by the deposition of collagen type 3 in the glomeruli. The absence of skeletal abnormalities in these patient is one feature that helps in distinguishing CG from nail patella syndrome, another collagen type 3 deposition disease in renal glomeruli. High serum levels of pro-collagen type III peptide were reported in this disease. Patients may have proteinuria, hematuria and/or renal dysfunction.
Gastric cancer (GC) is a leading cause of cancer-related death in the world and most patients have advanced disease upon presentation. The effect of age on prognosis in GC is controversial. We aimed to determine the impact of age on survival in patients with GC.This was a retrospective study of the medical records of Lebanese patients diagnosed with GC at the American University of Beirut Medical Center (AUBMC) between 2005 and 2014. Patients were divided into young (<65 years) and older groups (≥65 years). A multivariate analysis was done to determine the independent predictors of survival. Kaplan-Meier method was used for analysis of long-term survival outcomes.The sample consisted of 156 patients. The mean age was 62.15 (SD 13.54). Most patients presented with stage 4 disease (62.2%) and poorly differentiated histology (66.4%). The most common symptoms were abdominal pain and weight loss. On bivariate analysis, advanced stage (P=0.02) and higher grade (P=0.04) were associated with increased mortality. Patients <65 years of age were significantly more likely to have poorly differentiated tumours, while patients ≥65 years had more comorbidities (P=0.001). The 5-year DFS were 35% and 37% for patients <65 years of age and ≥65 years of age, respectively (P=0.15).Higher grade and advanced stage are associated with worse survival in patients with GC, but age did not seem to have an impact. Screening high risk patients and early diagnosis are necessary to improve survival.
Collagenofibrotic glomerulopathy (CG) is a rare disease characterized by the deposition of collagen type 3 fibrils in the glomeruli. Patients may have proteinuria, hematuria, and/or renal dysfunction. CG is considered a progressive disease with variable rates of progression. The definitive diagnosis is made by electron microscopy with the presence of characteristic subendothelial and mesangial curved, comma-like, banded collagen type 3 fibers of 40-65 nm periodicity. We are reporting the first case of CG in a kidney transplant recipient with kidney disease of unknown cause.
### Case Description
A 51-year-old man with ESKD secondary to FSGS on thrice weekly hemodialysis presented with an expanding painful right arm mass. He had long-standing secondary hyperparathyroidism with a persistently elevated PTH level > 2000 pg/ml and had been refusing to take calcimimetics or to undergo parathyroidectomy.
Physical examination demonstrated a hard and tender mass on the lateral aspect of the humerus.
An x-ray showed a 7.2×4-cm expanding lytic lesion with periosteal reaction (Figure 1). A skeletal survey showed similar smaller masses in the left humerus, left second metatarsal bone, and distal ulna together with few calcified soft tissue lesions in the right forearm, as well as partial Achilles tendon calcification and calcified abdominal aorta. A diagnosis …
The Gitelman and Bartter syndromes (GS and BS, respectively) are characterized by the constellation of hypokalemia, hypochloremia, metabolic alkalosis, hyperreninemic hyperaldosteronism, low to normal blood pressure and juxtaglomerular apparatus hypertrophy. These are due to pathogenic variants in the genes that encode the thiazide-sensitive sodium–chloride cotransporter NCC (SLC12A3) in the distal convoluted tubule or transporters involved in sodium chloride reabsorption in the loop of Henle. ‘Pseudo-Bartter syndrome’ (PBS) is caused by extrarenal or acquired renal salt losses and shares the same plasma electrolyte profile and acid–base disturbances, making the distinction from the genetic forms very challenging. PBS has various etiologies, including diuretic and laxative abuse, self-induced vomiting and the side effects of some antimicrobials. Additionally, congenital chloride diarrhea, cystic fibrosis, Pendred syndrome and chloride-deficient diet can manifest as PBS.
In this review we focus on factitious PBS secondary to diuretic abuse, laxative abuse or self-induced vomiting, whereby we point out some clinical and laboratory clues to help clinicians make the correct diagnosis.
