Haematuria

We collected data on the disease status (like renal histology, duration of nephrotic syndrome, number of relapses) and treatment status (like immunosuppressive treatments used before RTX, number of courses of RTX) of the patients. RTX response was measured at 1, 3, 6, 12, 18 and 24 months post RTX therapy in terms of proteinuria, spot urine protein/creatinine ratio (Up/Uc) or creatinine clearance. Complete blood counts, lipid profile and serum albumin levels were monitored regularly.

Nephritis is the inflammation of one or both kidneys. Causes may include: kidney conditions, lupus nephritis, neuropathy etc. Types of nephritis include: acute, chronic, glomerulonephritis, and autoimmune. Symptoms include: cloudy and bloody urine or reduced urine, and loin pain.

Similarly, patients with long-standing hypertension with hypertensive retinopathy and a family history of hypertension and CKD are likely to have hypertensive nephrosclerosis, particularly if urinalysis reveals minimal proteinuria and no hematuria22. It is worth noting that the presence of diabetes or hypertension does not rule out another cause of CKD, particularly since hypertension is a consequence of CKD. In addition, distinguishing between diabetic and hypertensive nephropathy is frequently challenging. However, a biopsy is usually not recommended because distinguishing between hypertension and diabetes as the underlying cause of CKD does not change management.

Initially, these symptoms appear intermittently and infrequently, but are most noticeable immediately after dialysis. Patients are often frustrated and disturbed by these symptoms. As result, they may often

Histopathologic sections will be examined in a blinded fashion for any evidence of pathology in the glomeruli. The glomeruli will be screened for evidence of crescent formation proliferative changes, fibrosis and basement membrane thickening. As described by Xie et al., 2004 the severity of type 1 RPGN will be graded on a 0-4 scale as follows: 0, normal; 1, mild increase in mesangial cellularity and matrix; 2, moderate increase in mesangial cellularity and matrix, with thickening of the GBM; 3, focal endocapillary hypercellularity with obliteration of capillary lumina and substantial increase in the thickness and irregularity of the GBM; and 4, diffuse endocapillary hypercellularity, segmental necrosis, crescents and hyalinized end-stage

According to the article URINARY TRACT INFECTIONS. (2012). “ Pyelonephritis is a and a common bacterial upper urinary tract infections in children, with recurrence being the highest concern in girls. The dominant causes of the infection are E.Coli, gram negative rods, and organisms that can enter the urethral tube and can damage the kidney or the lining of the urethra.” The bacterial infection enters into the bladder and advances into the kidneys causing an increase in fever, vomiting, apathy, and dysuria, which can lead to sepsis.

A very major point of concern is that the said disease appears to be the result of common viruses. The earlier symptoms of it can be narrowed down to usual fever and respiratory issues which then develop into muscle weakness and other AFM related

Glomerulonephritis is a group of diseases that injure the part of the kidney that filters blood (called glomeruli). Other terms you may hear used are nephritis and nephrotic syndrome. When the kidney is injured, it cannot get rid of wastes and extra fluid in the body. If the illness continues, the kidneys may stop working completely, resulting in kidney failure.

Therefore, starting treatment with penicillin at this time is not appropriate. Changes in urine and frequency of urination could be due to acute poststreptococcal glomerulonephritis, but there is typically a 1- to 2-week latent period between the onset of the throat infection and these changes. Therefore, the timeline in the vignette does not fit. Treatment with penicillin should also be avoided in this patient because penicillins are the second most common cause of drug-induced AIN behind

There are various defects associated with the kidney, which render it defective for its normal functioning. The main functions of these organs include regulating the pH of the body, osmoregulation, and production of hormones, regulating ion concentration and excretion of toxic substances among others. Once any part of the kidney is defective, these functions cannot be carried out as usual. As such, there is an urgency for a patient to seek medical advice as these functions are very crucial for the body to function properly. One of the major defects associated with kidney includes pyelonephritis. To understand this illness better, we will consider the case of Ms. Cornwall.

Nephrotic syndrome occurs when filtering units of the kidneys become damaged. As a result, protein which is usually kept in the plasma begins to leak into the urine in excessive amounts, which decreases the amount of protein in your body (Nephrotic Syndrome , n.d.). Nephrotic syndrome is caused by various disorders that can damage the kidneys. This damage results in too much protein being excreted in the urine. In addition to this, Nephrotic syndrome consists of various symptoms such as protein in the urine, elevated cholesterol levels, low blood protein levels in the blood, high triglyceride levels, and swelling. This condition can be diagnosed, upon arrival to the doctor’s office a physical exam will be performed. Laboratory tests will be

Glomerulonephritis (GN), or the inflammation of glomeruli, is a leading cause of renal failure worldwide. Inflammation is characterized by vascular fragility, infiltration of leukocytes, and edema. Glomerular disease may manifest by three major syndromes: nephritic syndrome, nephrotic syndrome, and rapidly progressive glomerulonephritis (RPGN). Nephritic syndrome consists of sudden onset of hematuria, non-nephrotic range proteinuria (1.5 g/24 h), active sediment with red blood cell (RBC) casts or dysmorphic RBCs, acute renal failure, and hypertension. Nephrotic syndrome is characterized by heavy proteinuria (>3.5 g/24 h), edema, hypoalbuminemia, and hyperlipidemia. RPGN is characterized by active sediment (RBC casts and dysmorphic RBCs) and rapid development of acute renal failure usually over a period of weeks to months. Glomerulonephritis accounts for the majority of progressive renal disease in many parts of the world.

One of the diseases is diabetes mellitus which is a major cause of renal failure. This disease can be defined as an increase of fasting blood glucose that is affected by a deficiency in insulin hormone. The normal range for glucose (fasting) in the blood is 2.8-6.0 mmol/L. It is classified into two groups, type 1 (insulin-dependent diabetes mellitus) and type 2 (non insulin-dependent diabetes mellitus). Stein (2008, p.6) points out that kidney failure happens most often when patients have suffered from diabetes mellitus for more than 10 years. According to United States Renal Data System (USRDS) report in 2007, approximately 44% of primary causes of renal failure is diabetes mellitus in the United States in 2005. Also, Stein (2008) indicates that 15% of dialysis patients are influenced by diabetes mellitus in the United Kingdom. Diabetes mellitus has negative affects throughout the kidneys where the increase of the range of blood sugar causes the damages to the cells in the kidneys. This leads to the presence of the glucose in the urine which is known as glycosuric.

Hemihypertrophy (OMIM:235000) Hemihypertrophy is uncommon medical disorder defined by the greater-than-normal asymmetry of the body. The one side of the body in hemihypertrophy is growing faster than the other side of the body. The condition may only affect one limb, finger, foot, face or the entire half of the body including the half of the brain and internal organs. Hemihypertrophy is generally a harmless condition although this depends on the part of the body that is affected. Patients with Hemihypertrophy are at increased risk of developing cancer. Symptoms of this disease are associated with other diseases, like Beckwith-Wiedemann syndrome (BWS), Proteus syndrome, Russell-Silver syndrome, and Sotos syndrome (Tricia Kinman and George Krucik, 2013).

On the other hand, we found that there was no significant relation between renalase level and the activity of LN, as our data for LN patients with active renal disease established no significant correlation between their serum renalase levels and the indicators of renal activity including ESR, proteinuria, P/C ratio, anti-dsDNA, C3, C4 and activity index of renal biopsy.