TERMINOLOGY CLINICAL CLARIFICATION5 • Hydronephrosis is the anatomic finding of dilated renal pelvis and renal calyces in one or both kidneys resulting from urinary obstruction, vesico-ureteral reflux (VUR), neurogenic bladder dysfunction, or as a congenital or acquired mega-ureter. • In common clinical usage the term hydronephrosis is used to indicate dilation of the ureter(s) as well as the renal pelvis, though technically that condition should be described as hydroureteronephrosis. CLASSIFICATION • International Reflux Study system6 ○ Grades of vesico-ureteral reflux and associated hydroureteronephrosis – One: reflux up to proximal ureter, slight dilation and tortuosity – Two: reflux into the renal pelvis, scant dilation and tortuosity – Three: reflux into the renal pelvis, notable dilation and tortuosity – Four: reflux into the renal pelvis with clubbing of renal calyces, significant dilation and tortuosity – Five: reflux into the renal pelvis, clubbing, dilation and distension of tortuous megaureter DIAGNOSIS CLINICAL PRESENTATION7 • History ○ The patient may be asymptomatic, complain of voiding symptoms (e.g., urinary frequency, urgency, nocturia), recurrent urinary tract infections or bladder spasm (intense involuntary contraction of the bladder) ○ Symptoms in children are vague and generalized in nature (e.g., "don 't feel good") ○ Fever, chills if urinary tract infection is present ○ Nausea, vomiting, abdominal pain or flank pain in acute obstruction (e.g.,
Kidney Disease - the kidney clean or filter the blood and produce urine waste material as
Injury to the glomerulus and the tubules presents the onset of Intra-renal failure (Matzke, 2011). Some of the frequent causes for Intra-renal failure are glomerulonephritis; pyelonephritis; and tubular injury. Post-renal failure develops from things like ureteroliths, tumors, or anatomic impediments. Opposite of the acute form, the chronic form has a slow onset that has no early stage symptoms. It is important to know that following an acute episode a chronic renal episode often follows, and at this juncture the damage is irreversible. Glomerulonephritis and pyelonephritis combined, has been reported to be the forerunner in as much as half the cases from acute to chronic renal failure. Diabetes mellitus, renal vascular disease, such as atherosclerosis, hypertension, polycystic kidney disease, drug damage, and nephrolith are all examples of other causes of CKD (Pradeep, 2014). Biopsies of kidneys that suffered with CKD reveal smaller kidneys with scarring on the tubules.
Kidney stones are hard, crystalline deposits in the kidney. They are usually hexagonal, eighty percent of which are made of calcium. These calcium stones are two to three times more common in men, and are most likely to reoccur. The calcium oxalate versions most likely result from eating specific food. One percent of stones are cystine stones, which have to do with
Nephritis is sometimes mistaken or misdiagnosed. So medical setting would start with primary care doctor testing through urine analysis, and then an urologist would do further testing. Medical settings include: kidney dialysis, nephrologists (kidney doctor), kidney and urinary health (urology, and nephrology).
A visit note from Dr. Robert Hendren (Urology), dated 09/20/2017, indicated that the claimant continued to have urinary frequency, urgency, and urge incontinence that required her 2 pads per day. She had microscopic hematuria noted on 08/31/2017. She had 3+ blood on urinalysis during the visit, but she had been undergoing her menstrual period. She had complaints of pain in the stomach, left arm, right leg, and foot. Urinalysis showed moderate blood with 30+ protein. Her BMI was 32.12. She was diagnosed with urge incontinence and hematuria. Cystoscopy was recommended.
| Term for any infection in the urinary tract, including cystitis and pyelonephritis. It can be
A 3.6 cm water density cyst off the anterior lower pole of the right kidney. Enhancing components not excluded in the absence of intravenous contrast. Ultrasound could be performed to confirm simple cyst as clinically warranted.
Further work up with computed tomography (CT) revealed a renal tumor (Figure 1.1) and a peri-urethral vaginal mass(Figure 1.2). The renal tumor was confirmed to be RCC, at which time she underwent a Laparoscopic Nephrectomy in February 2014. Subsequently she was referred to our service for evaluation of the vaginal mass.
On the same date an abdominal x-ray was also completed which revealed no small bowel dilation, no free gas, with a few small pelvis phleboliths (venous calcifications) noted. My involvement and care of the patient occurred Feb 22nd. On this date her lab work was: BUN 6.3, Cr 64, Na 138, K+ 3.5, Cl 107, C02 22, WBC 8.2 (15.4 Feb 15, 4.1 Feb 17), Hgb 93 (106 Feb 15, 80 Feb 16, 73 Feb 17), Hct .291, Plts 305. On assessment the client was still on contact plus isolation, but both a stool C+S and C-Diff tests were negative. Vitals: T 35.8, P 68 reg, RR 18, BP 94/52, Spo2 98% room air, Pain 0/10 (did receive 650mg acetaminophen @ 0630 for chronic Lt arm/hand pain).
obstruction to the kidneys, an imaging test which include CT scans or MRI to reveal a more
Hydronephrosis is when there is a disorder on one or both of the kidneys. The kidney starts to swell up due to urine back up and not able to filter out. But it can be caused by varies reason why it lead to this condition. Changing lifestyle by nutritional and exercises will help prevent chances of becoming kidney failure. Kidney function will begin decreasing immediately with the onset of hydronephrosis but is reversible if the swelling resolves. Usually kidneys recover if taking care of the obstruction right away even if it lasted for several weeks. Our kidneys have the most important job of filtering your blood. They remove waste products and extra
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.
Parenchymal echogenicity is the most frequently used marker for evaluating the presence of renal parenchymal disease. It is evaluated by comparing the echogenicity of the renal cortex, medulla and pyelic sinus with that of the adjacent liver and spleen (assuming that the liver and spleen present normal echogenicity). Echogenicity is divided into four different grades from 0 to III.9 However, the grading of parenchymal echogenicity does not differentiate between different histopathological conditions, and a normal renal echogenicity does not exclude that the patient’s kidney is damaged. In the evaluation of renal pathologies, sensitivity and specificity of echogenicity in grades I are 62% and 58%, respectively, whereas sensitivity and specificity of echogenicity in grade III are 20% and 96%, respectively.10 Parenchymal echogenicity varies also with the patient’s age (it is increased in newborn babies due to elevated cellularity and in elderly patients due to fibrosis). Increased cortical echogenicity has proved to correlate significantly with the prevalence of glomerular sclerosis, tubular atrophy, focal leukocyte infiltration, fluid retention, arteriosclerosis and with the presence of hyaline cylinders.11 These lesions are generally tubulointerstitial since the glomerular component accounts only for 8% of the renal parenchyma. Also the presence of diffused calcifications or precipitation of the calcium salts can increase the cortical echogenicity. The renal medulla can also appear hyperechoic, correlating histopathologically with the grade of medullary nephrocalcinosis, medullary tubular ectasia, medullary fibrosis, vascular congestion, and urate or protein deposits. The
Nephrotoxins, acute interstitial nephritis, glomerular damage, and vascular damage also correlate with intrarenal acute renal failure (Singh, Levy, & Pusey, 2013). Postrenal acute renal failure is usually a result of a urinary tract obstruction that affects the kidneys bilaterally, which causes the intraluminal pressure upstream from the site of the obstruction to increase with a progressive decrease in the glomerular filtration rate (McCance, Huether, Brashers, & Rote, 2014). A pattern consisting of several hours of anuria with flank pain followed by polyuria is typically found in individuals with postrenal acute renal failure (McCance, Huether, Brashers, & Rote, 2014).
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.