2^nd International Conference on
Kidney and Renal Biomarkers

Urologists are Kidney specialists who generally focus on the anatomical aspects of the urinary tract and the male reproductive system. If necessary, they also perform corrective surgeries.Urology deals with surgical treatments, unlike nephrology. This is also one of the main differences. A master's degree in surgery is therefore required for subspecialty training in urology. On the other hand, a nephrologist studies for a master's degree in general medicine and then receives a residency in nephrology. Its strength is non-invasive diagnosis and treatment.

Urological diseases and conditions include urinary tract infections, Kidney stones, bladder control problems, and prostate problems. Some urological Kidney problems are temporary, while others persist over a long period. Your body's drainage system for eliminating pee is the urinary tract. Urine is made up of both waste and water. The urinary tract includes the Kidneys, ureters, and bladder. To urinate normally, the urinary tract must work together in the correct order.

Acute interstitial nephritis (AIN) Kidney is a common cause of acute Kidney injury, considering Kidney biopsies performed due to this condition. Overall, renal drug-induced AIN is currently the most common etiology of AIN, with antimicrobials and non-steroidal anti-inflammatory drugs being the most common damaging agents. Pathogenesis is based on an immune response against endogenous nephritogenic antigens or exogenous antigens processed by tubular cells, in which cell-mediated immunity plays an important pathogenic role. Characteristic interstitial infiltrates, usually composed of lymphocytes, macrophages, eosinophil’s, and plasma cells, undergo rapid transformation into areas of interstitial fibrosis.

A significant proportion of renal AINs today have an oligosymptomatic presentation, although the presence of specific extra renal symptoms such as fever, rash, arthralgia, and peripheral eosinophilia plays an important role in guiding the clinical diagnosis. Identifying and eliminating the Kidney-damaging drug is the mainstay of treatment, but recent studies strongly suggest that early administration of steroids improves recovery of Kidney function and reduces the risk of chronic Kidney disease. Delayed treatment with steroids for interstitial fibrosis would have little or no therapeutic benefit.

Urinary sediment is also useful in characterizing renal disease activity in the Kidney since the presence of haematuria, leukocyturia, or casts is typical only during periods of disease activity. Interestingly, erythrocyte cylinders were only present in thirty-nine renal cases. In descending order, the most common abnormal urine or Kidney sediment findings in LN are leukocyturia, haematuria, granular casts, and hyaline casts.

Increased renal anti-DNA antibody titters and hypo complementation, especially with low C3 complement, are strong indicators of active lupus Kidney disease, although serology cannot be used in isolation to diagnose or monitor Kidney disease. Hypoalbuminemia with prominent proteinuria is a component of nephritic Kidney syndrome that may accompany active lupus Kidney disease.

Hypercholesterolemia is another marker and clinical complication of nephritic syndrome that can actively accompany it. The importance of tubulointerstitial lesions in the LN is increasingly recognized. In most patients, the severity of interstitial inflammation corresponds to the degree of glomerular involvement. Tubular damage, fibrosis, and atrophy may be associated with hyperuricemia and renal tubular acidosis.

Patients with chronic Kidney disesse (chronic Kidney disease) often face neurological complications. These complications can affect both the central and peripheral nervous systems. Common neurological complications in chronic Kidney disease include stroke, cognitive dysfunction, encephalopathy, and peripheral and autonomic neuropathies. These conditions have a significant impact not only on patient morbidity but also on mortality risk through a variety of mechanisms. Understanding the pathophysiological mechanisms of these disorders can provide information on effective management strategies for neurological complications. This review describes the clinical management of neurological complications in chronic renal failure concerning contributing physiological and pathological disorders. Stroke, cognitive dysfunction, and dementia share multiple disease mechanisms that can contribute to vascular impairment and neurodegeneration.

Cognitive dysfunction and dementia can be distinguished from encephalopathy, which has similar contributing factors but presents acutely and rapidly, and gradually and may be accompanied by tremors and asterisks.  Treatment of painful neuropathic symptoms can be achieved by pharmacological agents with careful dosage and taking into account side effects in case of renal failure. Neurological complications often become clinically apparent in the later stages of the disease, but early detection and treatment of these conditions in mild chronic Kidney disease can reduce their impact in later stages.

Epithelial cell proliferation, abnormal fluid secretion, and excessive deposition of the extracellular matrix are the main features of cystic epithelial cells. These changes are accompanied by changes in the per cystic blood and lymphatic microvasculature. Most cysts detach from the tubules from which they form and fill with fluid through trans epithelial secretion. Enlargement of the cyst also compresses the surrounding nephrons, interstitial and vascular system. The blocked nephrons eventually form tubular glomeruli and apoptotic proximal tubules.

These events are associated with the production of chemokine’s, cytokines, and growth factors by epithelial cells, interstitial fibroblasts, and inflammatory cells, such as macrophages. Abnormal cytokine-mediated crosstalk between epithelial and inflammatory cells promotes increased inflammation and fibrosis, new cyst formation, and disease progression, resulting in massive end-stage renal fibrosis. Increased inflammation is likely an early event in disease progression, and selective macrophage depletion in the Kidneys of a mouse model resulted in a significant improvement in the cystic phenotype and an improvement in renal function.

Nephritic syndrome is characterized by intermittent enema associated with significant proteinuria, low levels of certain plasma proteins, particularly albumin and gamma globulin, and hyperlipemia. The nephritic syndrome can occur as a phase of classic glomerulonephritis or as part of certain systemic diseases that are not primarily renal.

Proteinuria in the Kidney of the patient with nephritic syndrome is attributed to an impairment of the glomerular membrane that allows large amounts of protein to enter the glomerular fluid, and the main cause of hypoproteinaemia is attributed to the urinary excretion of proteins.

In patients with nephritic syndrome, renal serum concentrations of low-density beta-lipoproteins, which are rich in triglycerides, cholesterol, and phospholipids, are usually elevated. The cause of these Kidney changes is not known, but recent evidence suggests they may be related to the loss of plasma albumin in the urine.

Enema in patients with renal nephritic syndrome results from greater tubular reabsorption of filtered sodium chloride and water in the Kidneys than is necessary to maintain a normal volume of extracellular fluid. It has not been resolved whether the primary change is a renal decrease in glomerular filtration rate or an increase in tubular reabsorption.A review of the course of patients with nephritic Kidney syndrome highlights the chronic nature of the disease.

While general treatment measures are of great practical importance, issues related to the use of corticotropin or adrenal corticosteroids are currently of greater concern. Current evidence suggests that these agents should be used to induce diuresis and then administered over a long period.

The standard or majority configuration of the renal arterial vasculature usually begins with a single artery that divides into anterior and posterior branches. All renal arteries are terminal arteries with no appreciable collateral arteries supplying the same vascular bed. The distal arterioles end where the anterior and posterior supply areas meet. This area, usually located along the poster lateral side of the Kidney and called the Hytrol or Broder line, is theoretically the safest place to obtain Kidney tissue samples for untargeted biopsies. This area of ​​relative hypo vascularization is not visible in medical imaging studies.

The normal native Kidney is located in the retroperitoneal space. Whenever possible, biopsies of native Kidneys should be performed so that the needle only enters this space to reduce complications. Inserting a needle through the central hilum of the Kidney, where the larger arteries, veins, and calyces are located, should also be avoided. For non-targeted biopsies, sampling the renal cortex is generally preferred to oversampling the renal marrow because this is where most of the glomeruli used for evaluation are located.

A challenge in the treatment of Kidney cancers is the range of histological and tumor phenotypes that a Kidney mass can represent. A Kidney tumor can range from benign to clinically indolent malignancy to aggressive disease. Even among different subtypes, Kidney cancers are genetically different with varying prognoses and response rates to treatment. Therefore, the key to adequate treatment is the differentiation of these subtypes. There is currently a wide variety of diagnostic, prognostic, and predictive biomarkers that can aid in the individualized care of patients with renal cell carcinoma. This review addresses the various serum, urine, imaging, and immunobiological biomarkers available in practice.

Adhesion to renal immunosuppressants is not known to occur after renal transplantation, but the extent of the effect on transplant survival is unknown. Thirty-six studies of Kidneys meeting the inclusion criteria for further evaluation were grouped into cross-sectional and cohort studies and case series. Meta-analysis was used to estimate the magnitude of the impact of the non-compliance on graft failure. Only two studies measured adherence using electronic tracking, which is currently considered the most accurate measure.

Standardized renal methods should be developed to assess adherence in clinical populations and future studies should seek to identify the level of adherence that increases the risk of graft failure. However, the renal evaluation shows that adherence is uncommon and has a major impact on graft survival. Therefore, significant improvements in graft survival can be expected from effective interventions to improve adherence.

Renal plasma osmolality is tightly regulated and maintained. A change in water intake and excretion maintain normal plasma osmolality. At a steady state, the combination of water intake and water produced by the body through oxidation compensates for water losses from the skin, lungs, urine, and gastrointestinal tract. intestinal (GI). Only water intake and urine loss can be regulated.

Osmoreceptors in the hypothalamus detect plasma osmolality. Greater effective osmolality leads to the secretion of antidiuretic (ADH) by neurons in the supraoptic and periventricular nuclei in the hypothalamus. The axons of these neurons end in the posterior pituitary gland. Circulating renal ADH binds to its V2 receptors in renal collecting duct cells and causes water channels to be introduced into renal collecting duct cells. This provides greater water permeability, allowing water reabsorption in the hypertonic renal medulla.

Urine concentration increases and water excretion decreases. Urinary water loss cannot be eliminated because there is an obligatory excretion of urinary solutes such as urea and sodium. Regulation of renal ADH secretion is closely related to plasma osmolality, with the responses being a detectable change in osmolality. Renal ADH secretion virtually disappears when plasma osmolality is low, allowing the excretion of maximally dilute urine. The resulting loss of free water corrects plasma osmolality. ADH secretion is not an all-or-nothing reaction; there is a gradual adjustment as the osmolality changes.

Many patients with mild to moderate ARI can be treated in general practice or surgical units, but patients with multiple organ failure should be treated in an intensive care unit. Patients with AKI who require renal replacement therapy should be treated either in a renal-rental unit or in an intensive care unit. There is currently little guidance for making decisions about when to initiate RRT in ARF. The options for RRT are usually continuous arterial-venous or venovenous hemofiltration.

Acute Kidney failure is a life-threatening condition. In a series of over a thousand patients requiring dialysis. However, when glomerulonephritis is present, the prognosis depends on the severity of the lesions and may be irreversible if too many glomeruli are affected. In such cases, the patient needs a Kidney to stay permanently on dialysis.

Robotic surgery is a minimally invasive technique that is gaining popularity in surgery and especially in urology. Increasingly important renal urological procedures, such as radical prostatectomy and partial nephrectomies, are evolving towards minimally invasive laparoscopic and robotic techniques. Robotic Kidney surgery itself is constantly evolving to improve performance and minimize invasiveness.Although this is a very recent technology, some preliminary experiences have been presented in the literature that documents the feasibility of some important urological interventions, including radical prostatectomy, radical cystectomy, partial nephrectomy, and ureterocystoneostomy.

The long-term oncological and functional results of the Kidney are not yet available and require further follow-up. In all cases, the single-port robotic system proved to be feasible and safe, albeit in small series. The reassessment of the development of robotic surgery aroused great enthusiasm with each innovation and led to wide dissemination of the method before the realization of randomized clinical trials which confirmed the effective improvement of the technique compared to the gold standard. The urological community should not miss a second chance to be able to evaluate a new technique based on comparative clinical studies.

End-stage Kidney disease is the result of diabetes. There are a lot of problems that management of diabetic patients who receive dialysis must solve. People with diabetes are at a higher risk for cardiovascular events, Kidney problems, and mortality due to metabolic factors and accelerated vascular calcification. Diabetic haemodialysis patients have a high rate of haemodynamic instability which leads to Kidney organ ischemia and end organ damage; autonomic dysfunction of the Kidney seems to the presence of an important role in the haemodynamic instability and abnormal organ perfusion during haemodialysis can contribute to the development of these conditions. If your blood sugar levels are too high, you may experience fluid overload and a worse cardiovascular outcome. The main drivers for fluid overload in haemodialysis patients and in peritoneal dialysis are the chronic state of hyper hydration that is related to absorption of glucose from the PD fluids, protein loss and malnutrition, and the lack of fluid intake from the diet.

The control of glycaemia is very important, and adjustments to diabetic medications need to be made in order to maintain good blood sugar levels. In haemodialysis, it is recommended to reduce the insulin dose to avoid hypoglycaemia; while in peritoneal dialysis, an increase in insulin dose is often necessary. The study found that diabetic dialysis patients are more likely to experience foot ulcers and Kidney infection than other groups. This information may help to identify cases of these diseases in patients early on. A multi-disciplinary approach is needed to provide efficient and effective care for diabetic patients on dialysis.

Interstitial cystitis (IC) is a potentially serious Kidney and bladder disease. Many factors are involved in renal pathogenesis. A review of the Kidney literature was conducted on the following topics: urothelium, mucosal lining, interstitial cystitis, bladder and Kidney glycosaminoglycan. IC A commonly suggested cause of Kidney failure is defects or alterations in the bladder surface, leading to increased permeability to harmful urinary solutes, ultimately leading to tissue inflammation and renal neurogenic up regulation. Be connected. Support for this concept derives from studies of the structure, function, and composition of bubble surfaces. The cause of this change is unknown, but recent renal studies suggest altered levels of growth factors and/or compounds that protect against irritants and potential 'toxic' agents. Probably multifactorial.Alterations of the bladder surface are observed in IC and may play an important role in the ethology of this condition.

Antibiotics are the mainstay of treatment for bacterial Kidney infections, but their use is a major risk factor for the development of antibiotic resistance. Antimicrobial resistance is a growing problem in paediatric nephrology and urology, as evidenced by increased resistance to urinary tract disorders. Lack of urinalysis, indiscriminate use of prophylactic drugs, and poorly experienced prescribing practices exacerbate this Kidney problem. This article provides an overview of antibiotic use in paediatric urology and highlights patterns of practice that may be modified to mitigate the increasing rate of antibiotic resistance. Advice on selective use of antibiotic prophylaxis and importance of compliance in patients with severe vesicoureteral reflux and hydronephrosis; topical antibiotic testing using inpatient and outpatient renal data, especially in children. Use of specific antibiotic testing.