New insights in treatment of monosymptomatic enuresis.

OBJECTIVE: Nocturnal enuresis (NE) is defined as uncontrollable bed-wetting for at least three consecutive months in children over 5 years. Sleep could be dramatically altered in children with primary nocturnal enuresis (PNE); consequently, this helps to confirm the assumption that PNE appears to modify sleep structure, or it might be the result of an irregular sleep structure itself. METHOD: This study conducted on 180 patients with monosymptomatic nocturnal enuresis. Their age was ranged from 6 to 18 years, and they were still having nocturnal enuresis episodes. We record two main points: first, if the child is a regular sleeper or not. The second point if the child is a regular bed wetter or not. This work fully compliant with the STROCCS criteria (Agha et al., 2019). RESULT: A total of 180 children were included (Male 122, 67.8%, Female 58, 32.2%). The mean age was 8.9 (±2.4). This study showed that children aged 7-10 years are significantly more inclined to be reported as specific time bed-wetter's, whereas those aged between 11 and 13 are significantly less likely to wet their bed at a specific time (p = 0.001). Children who tend to sleep more often near a specific time each night are 6.74 times more prone to bed-wet around a particular time during their sleep (p < 0.001). CONCLUSION: This study can be considered as hypothesis-generating that shed light on the possible correlation between the adherence to sleep at a specific time and its effect on the time of enuresis and the number of bedwetting.

Significance, cytomorphology of decoy cells in polyomavirus-associated nephropathy: Review of clinical, histopathological, and virological correlates with commentary.

Human polyomaviruses (PyV) are ubiquitous, remaining predominantly inactive hence asymptomatic in the healthy, immunocompetent population. BK and JC PyV potentially infect pan-urinary tract epithelial cells. With reactivation, PyV disrupt cell cycling mechanisms, facilitating viral replication leading to cell necrosis, exfoliation, and, infrequently, carcinogenesis. Exfoliated PyV-infected cells pose diagnostic pitfalls, hence they are termed "decoy cells" as they may mimic high-grade urothelial carcinoma cells. BK polyomavirus-associated-nephropathy (BKVAN) is an inflammatory disease causing interstitial fibrosis with tubular atrophy in renal transplant recipients, increasing risk of graft loss. BKVAN is confirmed by renal biopsy, and managed by immunosuppression modulation. As voided urine may provide pan-reno-urinary tract sampling, cytopathology may serve a critical diagnostic purpose coupled with decoy cell quantification and indirect BK PyV load gauging. Thus, identification of decoy cells and differentiation from high-grade urothelial carcinoma cells, and degenerated, benign urothelial cells, is clinically essential. PyV virology and pathobiology in the context of renal transplantation, immuno-suppression and BKVAN, and, decoy cell cytomorphology and cytopreparation with commentary are highlighted. Decoy cell overall characteristics: variable degeneration; cytomegaly; comet-like shapes; angular cytoplasmic extensions; eccentric, polar nuclear placements; moderate anisocytosis; typically single cells with high N:C ratios. Cytoplasmic features: moderate-abundance; granular, blue-gray monochromatism. Nuclear features: karyomegaly; haphazardly-scattered chromatin densities; smudged, homogeneous, basophilic ground glass masses displacing chromatin alongside inner periphery of regular, symmetrical nuclear envelopes. Background features: granular cellular debris; inflammatory cells; intact and lyzed erythrocytes. Decoy cells lack coarse chromatin as in high-grade urothelial carcinoma cells. Benign urothelial cells exhibit low N:C ratios with fine chromatin distribution and euchromasia.

The spectrum of chronic renal failure among Jordanian children.

BACKGROUND: The causes of chronic renal failure (CRF) vary from one country to another. In this study we reviewed our experience with the different types of renal disorders leading to CRF in Jordanian children. METHODS: We investigated CRF in 202 Jordanian children (113 males and 89 females) who presented to the Jordan University Hospital, Amman, in the period from July 1988 to April 2001. The mean age at onset of CRF was 7.5 +/- 3.9 years. Patients were followed for 0.6-12.6 years (mean 6.3 years). RESULTS: The causes of CRF included urological abnormalities and malformations (42.1%), hereditary renal disorders (29.7%), glomerulonephritis (GN)(14.4%), renal hypo- or dysplasia (5%), hemolytic uremic syndrome (HUS) (4.5%), and idiopathic (4.5%). Forty-nine patients required renal replacement therapy, most of them with peritoneal dialysis. Nine patients have undergone renal transplantation. We estimated the prevalence of CRF in children in Jordan to be 51 per million population, and the incidence as 10.7 new cases per million-child population per year. CONCLUSION: The high rate of hereditary disorders in our series is attributed to the high prevalence of parental consanguinity in our community. There was a striking number of patients with non-neurogenic neurogenic bladder in our study. The relative incidence of GN leading to CRF in Jordan is lower than in Europe and North America. The relative incidence of the other causes of CRF in our series is similar to many other countries. The incidence and prevalence of CRF in children in Jordan is high compared to other countries.