Subtypes

• glomerulonephritis is inflammation of the glomeruli. (Often when the term "nephritis" is used without qualification, this is the condition meant.)

• interstitial nephritis or tubulo-interstitial nephritis is inflammation is of the spaces between renal tubules.

• pyelonephritis is when a urinary tract infection has reached the pyelum (pelvis) of the kidney.

• Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system.

Glomerulonephritis, also known as glomerular nephritis and abbreviated GN', is a primary or secondary immune-mediated renal disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys. It may present with isolated hematuria and/or proteinuria (blood resp. protein in the urine); or as a nephrotic syndrome, a nephritic syndrome, acute renal failure, or chronic renal failure. They are categorised into several different pathological patterns, which are broadly grouped into non-proliferative or proliferative types. Diagnosing the pattern of GN is important because the outcome and treatment differs in different types. Primary causes are one which are intrinsic to the kidney, whilst secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), drugs, systemic disorders (SLE, vasculitis) or cancers.

Pyelonephritis is an ascending urinary tract infection that has reached the pyelum (pelvis) of the kidney (nephros in Greek). If the infection is severe, the term "urosepsis" is used interchangeably. It requires antibiotics as therapy. It is a form of nephritis. It can also be called pyelitis.

Pathology

Acute pyelonephritis is an, exudative purulent localized inflammation of kidney and renal pelvis. The renal parenchyma presents in the interstitium abscesses (suppurative necrosis), consisting in purulent exudate (pus): neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). Tubules are damaged by exudate and may contain neutrophil casts. In the early stages, glomeruli and vessels are normal.[1] Gross pathology often reveals pathognomonic radiations of hemorrhage and suppuration through the renale pelvis to the renale cortex. Chronic infections can result in fibrosis and scarring.

Chronic pyelonephritis is often caused by Xanthogranulomatous pyelonephritis.

Causes

Ascending bacteria (such as E.coli) from lower urinary tract infections, mainly cystitis and prostatitis. true....

Signs and symptoms

It presents with high spiking fever, backache, vomiting, dysuria (painful voiding), rigors and often also with confusion. There may be renal angle tenderness on physical examination.

Diagnosis

Nitrite and leukocytes on a urine dipstick are often detected, which may be an indication for empirical treatment. Formal diagnosis is with culture of the urine and bloods.

In patients with recurrent ascending urinary tract infections, it may be necessary to exclude an anatomical abnormality, such as vesicoureteric reflux (urine from the bladder flowing back into the ureter).

Treatment

Treatment is with antibiotics, which are often administered intravenously to improve the effect. Trimethoprim (or co-trimoxazole) or nitrofurantoin are often used first-line, although in full-blown pyelonephritis amoxicillin (with or without clavulanic acid), gentamycin (with or without ampicillin), fluoroquinolones (eg. ciprofloxacin) or a third generation cephalosporins are often favoured.

RENAL CALCULI

Acute passage of a kidney stone from the renal pelvis through the ureter gives rise to pain at times so excruciating that it has been likened to the discomfort of childbirth. The often sudden, extremely painful episode of renal colic prompts more than 450,000 visits to EDs annually and places emergency physicians on the front line of management of acute nephrolithiasis. ED management is focused on excluding other serious diagnoses and providing adequate pain relief.

Pathophysiology: Most calculi arise in the kidney when urine becomes supersaturated with a salt that is capable of forming solid crystals. Symptoms arise as these calculi become impacted within the ureter as they pass toward the urinary bladder.

Acute passage of a kidney stone from the renal pelvis through the ureter gives rise to pain at times so excruciating that it has been likened to the discomfort of childbirth. The often sudden, extremely painful episode of renal colic prompts more than 450,000 visits to EDs annually and places emergency physicians on the front line of management of acute nephrolithiasis. ED management is focused on excluding other serious diagnoses and providing adequate pain relief.

Pathophysiology: Most calculi arise in the kidney when urine becomes supersaturated with a salt that is capable of forming solid crystals. Symptoms arise as these calculi become impacted within the ureter as they pass toward the urinary bladder.

Emergency Department Care:

• Intravenous access should be obtained to facilitate delivery of analgesic and antiemetic medications.

• Intravenous hydration is controversial.

• Some authorities believe that intravenous fluids hasten passage of the stone through the urogenital system. Others express concern that additional hydrostatic pressure exacerbates the pain of renal colic.

• No data exist to support either theory. Intravenous hydration should be given to patients with clinical signs of dehydration or to those with a borderline serum creatinine level who must undergo IVP.

• Analgesia should be provided promptly.

• The pain of renal colic is mediated by prostaglandin E2. Nonsteroidal anti-inflammatory drugs inhibit formation of this mediator, and ketorolac (the only parenteral NSAID approved by the FDA) has been proven in multiple studies to be as effective as opioid analgesics, with fewer adverse effects.

• Opioid analgesics can be added in cases of incomplete pain control.

• Antiemetics should be administered as needed.

• Medical expulsive therapy

• Multiple prospective randomized controlled studies (Dellabella, 2003; Dellabella, 2005; Porpiglia, 2004) have demonstrated that patients treated with oral alpha-blockers have an increased rate of spontaneous stone passage and a decreased time to stone passage. The best studied of these is tamsulosin, 0.4 mg administered daily.

• Calcium channel blockers in combination with oral steroids have also proven efficacious in multiple studies. The most common regimen is 30-mg slow-release nifedipine daily plus oral corticosteroid such as prednisolone.

• Strain urine for stone collection.

Consultations:

• Consult a urologist immediately in cases of ureterolithiasis with proximal UTI. Infected hydronephrosis is a true urologic emergency and requires hospital admission, intravenous antibiotics, and immediate drainage of the infected hydronephrosis via percutaneous nephrostomy or ureteral stent placement.

• Urologic consultation is also appropriate in patients who are unable to tolerate oral fluids and medications and in those with unrelenting pain, renal failure, renal transplant, a solitary functioning kidney, and history of prior stones that required invasive intervention.

Renal failure or kidney failure is the condition in which the kidneys fail to function adequately.

Biochemically, it is typically detected by an elevated serum creatinine. In the science of physiology, renal failure is described as a decrease in the glomerular filtration rate