Chronic kidney disease (CKD) is a progressive condition characterized by a continuous decline in renal function, independent of the initial cause of damage or external factors such as infection, inflammation, or toxins. The accurate measurement of renal function, typically assessed using the glomerular filtration rate (GFR), is crucial for managing CKD. The most accepted hypothesis for CKD progression is glomerular damage caused by hyperfiltration. Various factors can accelerate CKD progression, and several biomarkers have been identified to monitor this progression. Numerous studies have explored the risk factors associated with CKD progression, and some of these factors can be modified. Additionally, several drugs are now available that can reduce CKD progression. This review summarizes recent publications and highlights potential future research directions in CKD progression. It discusses the evolution of GFR measurement methods, the mechanisms driving CKD progression, and the latest findings on biomarkers and risk factors. Furthermore, it explores therapeutic strategies, including dietary modifications and pharmacological interventions, to slow CKD progression. Understanding these mechanisms and interventions is crucial for developing effective therapeutic strategies to prevent or slow CKD progression.
Urinary tract infections (UTIs) are common bacterial infections in children. UTIs may be limited to the bladder or involve the kidneys with possible irreversible damage. Congenital abnormalities of the kidney and urinary tract (CAKUT) are often associated with UTIs; kidney scars have been considered a consequence of untreated UTIs but may be congenital. The mechanism by which bacteria produce inflammation in the urinary system has been intensively investigated. Diagnostic tools, including invasive imaging procedures, have been advocated in infants and small children with UTIs but are not necessary in most cases. Effective antibiotic drugs are available, and prophylactic treatment has been questioned. Several guidelines on UTIs are available, but a simple one for general practitioners is needed.
7 September 2010 in The Journal of Maternal-Fetal & Neonatal Medicine
Observational studies in humans and experimental studies in animals have clearly shown that renal failure may start early in life. ‘Fetal programming’ is regulated by adaptations occurring in uterus including maternal nutrition, placental blood supply, and epigenetic changes. Low birth weight predisposes to hypertension and renal insufficiency. Congenital abnormalities of the kidney and urinary tract, adverse postnatal events, wrong nutritional habits may produce renal damage that will become clinically relevant in adulthood. Prevention should start early in children at risk of renal disease.
Background: A great majority of children with idiopathic nephrotic syndrome will relapse after successful treatment of the initial episode. The possibility that different steroid dosing regimens at onset, adjusted for risk factors, can reduce the rate of relapse represents an interesting option to investigate.Objectives: To evaluate the effect of the initial steroid regimen, adjusted for time to remission (TTR), on the frequency of relapses and steroid dependence, and to verify the influence of prognostic factors on disease course.Methods: A multicentre, prospective, cohort study. Children with nephrotic syndrome, with TTR ≤ 10 days (Group A), were given a 20-week prednisone regimen (2,828 mg/m2) and those with a TTR >10 days, a 22-week regimen (3,668 mg/m2) (Group B). Previously published retrospective data from the same centers were also evaluated. Main outcomes were: relapse rate, number of frequent relapsers + steroid dependent children and total prednisone dose after induction.Results: 143 children were enrolled. Rate of relapsed subjects (77 vs. 79%) and frequent relapsers + steroid dependent subjects (40 vs. 53%) did not differ between Groups A and B, or between the retrospective and prospective cohorts. The cumulative prednisone dose taken after the induction treatment was similar in both groups and in the retrospective and prospective cohorts. TTR was not associated with relapse risk. Age at onset and total serum protein were significantly lower in relapsing patients. At ROC analysis, the best cut-off was 5.3 years for age at onset and 4.2 g/dL for total serum protein. According to these cut-offs, older children with higher total serum protein had a higher relapse free survival rate (58%) than younger children with lower total serum protein (17%).Conclusions: TTR was not found to be a prognostic factor of relapse; because of this, different steroid regimens, adjusted for TTR, did not modify the relapse rate in any relevant measure. Conversely, younger age and low total serum protein were independent predictors of relapse risk, however this outcome was not modified by higher prednisone regimens.Clinical Trial Registration:https://www.ClinicalTrials.gov/, identifier: NCT01386957 (www.nefrokid.it).
Vesicoureteral reflux (VUR) is associated with urinary tract infections (UTI) and renal scars. The kidney damage is correlated with the grade of reflux and the number of UTI, but other factors may also play a role. Uromodulin (UMOD) is a protein produced by kidney tubular cells, forming a matrix in the lumen. We evaluated whether the common variant rs4293393 in the UMOD gene was associated with febrile UTI (FUTI) and/or scars in a group of children with VUR. A total of 31 patients with primary VUR were enrolled. Renal scars were detected in 16 children; no scar was detected in 15 children. Genotype rs4293393 TC (TC) was present in 8 patients, 7 (88%) had scars; genotype rs4293393 TT (TT) was found in 23 patients, and 9 (39%) had scars. Among children with scars, those with TC compared with those with TT were younger (mean age 77 vs. 101 months), their reflux grade was comparable (3.7 vs. 3.9), and the number of FUTI was lower (2.9 vs. 3.7 per patient). Children with VUR carrying UMOD genotype rs4293393 TC seem more prone to developing renal scars, independent of FUTI.
Congenital anomalies of the kidney and urinary tract (CAKUT) are a common cause of chronic kidney disease in children. Most patients will reach end-stage renal function and dialysis or transplantation in childhood or early adulthood. Patients with CAKUT deserve a careful evaluation before a kidney transplant; detailed imaging and functional studies are necessary, particularly in the presence of lower urinary tract abnormalities, and surgical procedures are advisable in selected cases. A higher incidence of complications has been reported after a kidney transplant in CAKUT, mainly urinary tract infections. However, in the long term, the prognosis seems to be comparable to other kidney diseases. A large number of reports are available in the literature on medical and surgical management of patients with CAKUT before, during, and after a kidney transplant; almost all recommendations of surgical procedures before a kidney transplantation are based on retrospective not controlled studies or personal opinions; prospective controlled studies are needed. In this narrative, nonsystematic review, we report the results of recently published selected studies and underline questions that should be addressed in future guidelines.