Your kidneys are two bean-shaped organs, each about the size of your fist. They are located in the middle of your back, just below your rib cage, on either side of your spine. The right kidney is situated lower than the left kidney. The costovertebral angle is an external landmark useful for locating the kidneys. Your kidneys weigh about 0.5 percent of your total body weight. Although the kidneys are small organs by weight, they receive a huge amount -- 20 percent -- of the blood pumped by the heart. The large blood supply to your kidneys enables them to do the following tasks:

• Regulate the composition of your blood

• Keep the concentrations of various ions and other important substances constant

• Keep the volume of water in your body constant

• Remove wastes from your body (urea, ammonia, drugs, toxic substances)

• Keep the acid/base concentration of your blood constant

• Help regulate your blood pressure (renin-angiotension)

• Stimulate the making of red blood cells (renin-angiotension)

• Maintain your body's calcium levels

­­Your kidneys receive the blood from the renal artery, process it, return the processed blood to the body through the renal vein and­ remove the wastes and other unwanted substances in the urine. Urine flows from the kidneys through the ureters to the bladder. In the bladder, the urine is stored until it is excreted from the body through the urethra. Each kidney contains around a million units called nephrons, each of which is a microscopic filter for blood. It's possible to lose as much as 90% of kidney function without experiencing any symptoms or problems.

Urinary tract obstruction can occur at any point in the urinary tract, from the kidneys to the urethral meatus. The obstruction may be bilateral or unilateral, partial or complete, and occur sudden or gradually. It can develop secondary to calculi, tumors, strictures, and anatomical abnormalities. Obstructive uropathy can result in pain, urinary tract infection, loss in renal function, or, possibly, sepsis or death. Chronic urinary tract obstruction can lead to permanent damage to the urinary tract. Progressive back pressure on the ureters and kidneys can occur and can cause hydroureter and hydronephrosis. The ureter can then become dilated and tortuous, with the inability to adequately propel urine forward. Hydronephrosis can cause permanent nephron damage and renal failure. Urinary stasis along any portion of the urinary tract increases the risk of stone formation and infection, and, ultimately, upper urinary tract injury. Urinary tract obstruction can cause long-lasting effects to the physiology of the kidney, including its ability to concentrate urine.

Obstruction that occurs anywhere along the upper urinary tract will lead to increased pressure within the structures of the kidney due to the inability to pass urine from the kidney to the bladder.

• Obstruction of the upper urinary tract causes dilation of the ureter (hydroureter), enlargement of the renal pelvis and calyces (hydronephrosis), or both (ureterohydronephrosis). This is a response to obstruction that leads to smooth muscle hypertrophy and urinary stasis above the blockage. Unless relieved, it can lead to enlargement of the nephron and damage to the tubules. This can cause the kidney to be unable to concentrate urine and a reduced glomerular filtration rate (GFR), although this may take some time to develop.

• Obstructive processes result in urine stasis, which predisposes to infection and structural damage. Common causes of obstruction include stones, tumors, prostatic hypertrophy, and strictures of the ureters or urethra. Of all potential causes, renal stones are the most common.

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  Complete obstruction results in hydronephrosis, decreased GFR, and ischemic kidney damage because of increased intraluminal pressure. Prolonged postrenal acute renal failure due to the obstruction may result in acute tubular necrosis (intrarenal acute renal failure) and chronic kidney disease.

• Stones tend to form in the urinary tract under conditions of solute supersaturation, low urine volume, and abnormal urine pH. Certain factors increase the risk of stone formation, while others act as inhibitors.

• Most stones are composed of calcium crystals. Other forms include uric acid, struvite, cystine, and stones that form in association with certain medications.

• Stationary stones in the renal pelvis are generally asymptomatic. When the stone migrates to the junction with the ureters and beyond, intense renal colic pain ensues. Pain is usually abrupt in onset and may radiate. Additional signs and symptoms include nausea, vomiting, and diaphoresis.

The enlarged kidney.

due to an immune response to a variety of potential triggers and may have a primary or secondary etiology. Attraction of immune cells to the area of inflammation results in lysosomal degradation of the basement membrane. The GFR may fall, in part because of contraction of mesangial cells resulting in decreased surface area for filtration.

may be classified as acute or chronic. Acute (rapidly progressive, poststreptococcal) forms are usually triggered by infection (strept infection). Signs of specific glomerular injury that does not have a specific cause. Characterized by the abrupt onset (a matter of months) of varying degrees of hematuria, proteinuria, oliguria and azotemia, edema, and hypertension. Immune complex disorders such as small vessel vasculitides and goodpasture syndrome. Chronic forms are those that slowly progress to chronic kidney disease over a period of years. With chronic glomerulonephritis some people have no history of glomerular disease. Present with persistent proteinuria, with or without hematuria and slowly declining renal function. It is characterized by small kidneys with sclerosed glomeruli.

can damage your kidneys so that they lose their filtering ability. This can lead to the accumulation of dangerous levels of fluid, electrolytes and waste in your body (called kidney failure) and deprive your bloodstream of necessary protein.

Antigen-Antibody Complex in Glomeruli Causing: Inflammation, decreased GFR.

From recent strep infection.

S/S: HA, elevated BP, facial/periorbital edema, lethargic, low grade fever, weight gain, proteinuria, hematuria, oliguria, dysuria.

Crystallization and stone formation occurs with many solutes found in urine and may be promoted or inhibited by a number of factors. Kidney stone formation requires a supersaturated (saturated with stone components) urine and an environment that allows the stone to grow.

Risk factors: infection, urinary stasis and retention, immobility, dehydration, increased uric acid, increased urinary oxalate.

Calcium stones are most common. Calcium can combine with other substances, such as oxalate (the most common substance), phosphate, or carbonate to form the stone. Associated with increased concentrations of calcium in the blood and urine. Oxalate is present in certain foods. Diseases of the small intestine increase the risk of forming calcium oxalate stones.

• Cystine stones can form in people who have cystinuria. Genetic predisposition.

• Struvite stones/Magnesium ammonium phosphate stones form in alkaline urine and in the presence of bacteria that possess a specific enzyme. Associated with urinary tract infections. These stones can grow very large and can block the kidney, ureter, or bladder.

• Uric acid stones occur with gout and high concentrations of uric acid in the urine.

The main symptom is severe pain that starts suddenly and may go away suddenly: Pain may be felt in the belly area or side of the back. Pain may move to groin area or testicles. Other symptoms can include: Abnormal urine color, Blood in urine,Chills, Fever, Nausea, Vomiting, Colicky pain- pain that accompanies stretching of the collecting system or ureters. N/V, agonizing flank pain that may radiate to: groin, testicles, abdominal area. Sharp, sudden severe pain, hematuria, dysuria, urinary frequency,

An inflammation caused by bacteria that primarily affects the interstitial area and the renal pelvis or the renal tubules.

Risk factors: those that increase the host's susceptibility or reduce the host's response to infection (diabetes), catheterization, urinary instrumentation, vesicourerteral reflux, pregnancy, and neurogenic bladder.

S/S: Abrupt onset of shaking chills, moderate to high fever, a constant ache in the loin area of the back that is unilateral or bilateral, dysurea, frequency, malaise, n/v, abdominal pain, costovertebral angle pain, and pyuria.

Patho: infection of the upper urinary tract, specifically the renal parenchyma and renal pelvis. infection usually ascends from the lower urinary tract

often occurs after a lower urinary tract infection but can occur independently.

Other predisposing factors include vesicoureteral reflux, pregnancy, diabetes, neurogenic bladder, instrumentation (e.g., catheterization, cystoscopy), and female sexual trauma.May affect one or both kidneys.

Bacterial colonization occurs in the renal papilla as a result of increased osmolarity of urine containing organisms; increased osmolarity interferes with white blood cell (WBC) and complement function, allowing bacteria to multiply.

• Abscesses can form, particularly if the causative organism is Staphylococcus.

• In the absence of obstructive uropathy, usually only one kidney is involved; however, if obstruction (e.g., gravid uterus, renal calculi, prostatic hypertrophy) is present, the potential exists for both kidneys to become infected.

Symptoms may include fever, chills; achiness, flank ache or pain, anorexia and abdominal pain accompanied by nausea, vomiting, and fatigue.

• The hallmark sign is tenderness or pain at the costovertebral angle on palpation.

• Lower urinary tract symptoms, such as frequency and urgency of urination or hematuria, may or may not be present.

• Urinalysis usually shows WBCs and occasional red blood cells (RBCs), and it may show WBC casts. A complete blood cell count may show an elevation in the total WBC count.

can potentially result in chronic kidney disease. It is usually associated with vesicoureteral reflux or obstructive processes leading to persistent urine stasis. Ongoing inflammation causes fibrosis and scarring and loss of functional nephrons.