Papillary necrosis of the kidney

Characterized by coagulative necrosis of the renal medullary pyramids and papillae.

Usually affects individuals who are in the middle decades of life or older, with nearly half of cases occurring in individuals older than 60 years.

More than 90% of cases occurring in individuals older than 40 years.

Uncommon in the pediatric age group , except in patients with sickle cell hemoglobinopathies, hypoxia, dehydration, and septicemia.

More common in women than in men.

In patients with diabetes, women outnumber men, and in patients without diabetes, men outnumber women, reflecting the significance of urinary tract obstruction in elderly in men.

Acute or chronic pyelonephritis demonstrated at autopsy in 95% of patients with RPN.

Occupational risks are not associated with developing renal papillary necrosis.

Associated with clinical conditions and toxins that lead to the development of ischemia.

Prognosis depends on the degree of vascular impairment, the causal factors, the overall health of the patient, the presence of bilateral involvement, and the number of affected papillae.

Can lead to secondary infection of necrotic foci, deposition of calculi, and eventual sloughing of papillae, with impending acute urinary tract obstruction.

Sloughing of papillae can obstruct calyces or can embolize to more distal sites such as the ureteropelvic junction, ureter, or ureterovesical junction.

With bilateral involvement or an obstructed solitary kidney, may lead to renal failure.

The infectious complications are more serious if the patient has multiple medical problems, particularly diabetes mellitus.

17-90% of all patients with renal papillary necrosis have diabetes and that 25-73% of patients have severe urinary tract obstructions.

Analgesic abuse has been increasingly associated, and is also more common in women than in men with recurrent headaches, muscle and joint pain, and in patients with underlying psychologicall problems.

Sometimes associated with pyelonephritis and tubulointerstitial nephritis, and is often considered a complication or extension of severe pyelonephritis.

However, renal papillary necrosis does not usually occur with florid pyelonephritis.

Infection is a frequent and is associated with fever and chills in 2/3 of patients, positive urine culture results in 70%.

Papillary necrosis can occur in the absence of infection.

Infection is likely a complication of renal papillary necrosis as the necrotic papillae act as a nidus for infection and stone formation.

Infection often recurs as renal papillary necrosis progresses to chronic pyelonephritis.

Renal papillary necrosis is a result of ischemia in the renal papillae and the medulla.

Ischemia is caused by a number of processes, including infection.

Interstitial kidney inflammation compresses the medullary vasculature and, thus, predisposes the patient to ischemia and renal papillary necrosis: infection diabetes mellitus, urinary tract obstruction, and analgesic nephropathy may be responsible.

RPN associated with several diseases that predispose a patient to ischemia.

Mostly a bilateral process, given the systemic nature of the associated diseases and the ischemic pathophysiology.

When a single kidney is involved at initially, the contralateral kidney will develop RPN within 4 years.

Unilateral RPN is diagnosed when the patient’s predisposing factor is infection or obstruction that is limited to one kidney,.

Associated with any process associated with ischemia such as shock, massive fluid sequestration, dehydration, hypovolemia, and hypoxia.

More than half the patients have 2 or more causative factors, indicating that in most patients the process is multifactorial in origin.

The five most frequently associated conditions are infection, obstruction, diabetes mellitus, analgesic abuse, and sickle cell disease.

The presence of multiple conditions worsens both the severity of the disease and the prognosis.

In patients with renal hypoperfusion, local prostaglandin synthesis protects the glomeruli and tubules from ischemia, and inhibition of prostaglandin synthesis by NSAIDs that inhibit COX-1 and, COX-2, removes this protective mechanism and predisposes the kidney to further renal hypoperfusion and, ischemia.

Renal papillary necrosis is classified as focal or diffuse, depending primarily on the patient’s degree of impaired vasculature.

Focal RPN involves only the tip of the papilla.

Diffuse RPN involves the whole papilla.

Renal papillary necrosis never involves the entire medulla.

The process is limited to the inner, more distal zone of the medulla and the papilla.

There are 2 pathologic forms of renal papillary necrosis, the medullary form and the papillary form, based on the degree of vascular impairment.

The medullary form is characterized by intact fornices, discrete tiny necrotic areas, and later defects in the papillae.

In the papillary form, the calyceal fornices and the entire papillary surface are destroyed.

Medullary ischemia results in decreased glomerular filtration rates, salt wasting, impaired ability to concentrate, and polyuria as the the vasa rectae are needed for the countercurrent exchange mechanism.

Pathology findings reveal gray-white-yellow necrosis on the tips or distal two thirds of the pyramids, coagulative infarct necrosis, with preserved tubule outlines.

Leucocytes invade the junctions between preserved and destroyed tissue.

Following acute disease scars develop on the cortical surface and replace the inflammatory foci, and they are associated with inflammation and a deformation of underlying calyces and pelvis.

The papillae show necrosis, calcification, fragmentation, desquamation, and sloughing.

Tubules and calcifications subsequently fragment, slough, and can become obstructive.

Patients present with a variable clinical course that ranges from a chronic, and relapsing form to an acute, rapidly progressive form.

The acute progressive form is rare, and can result in death from septicemia and renal failure.

The chronic form Is more common chronic and patients may remain asymptomatic until diagnosed incidentally or by the passage of sloughed papillae in the urine.

The symptomatic chronic form manifests as episodes of pyelonephritis with hydronephrosis.

Chronic form can simulate nephrolithiasis.

Symptomatic papillary necrosis commonly manifested by presentation with fever, chills, flank and/or abdominal pain, and hematuria.

Acute renal failure with oliguria or anuria are rare events.

The sudden deterioration in renal function in a patient with diabetes or in a patient with a known history of chronic obstruction and/or pyelonephritis the diagnosis of papillary necrosis is a consideration.

Acute ureteral obstruction from sloughed papillae may occur and is manifest by flank pain and ureteral colic due to hydronephrosis or pyonephrosis

Hematuria is invariably present.

Pyelonephritis can complicate the presentation with fever, chills, prostration, and sepsis.

The differential diagnoses of flank pain or hematuria includes: infectious, neoplastic, congenital, metabolic, and hematogenous processes.

Blood coagulum downstream from a bleeding source in the kidney (eg, renal cell carcinoma, angioma, angiomyolipoma, arteriovenous malformation, trauma to a pyelonephritic or multicystic kidney) can also manifest with a similar clinical picture. If a patient has acute ureteral obstruction with fever and leukocytosis, the pref2242ed treatment is drainage of the system.

Pyonephrosis may or may not be present; therefore, the initial short-term management of an obstructed system should be conservative, with resuscitation, drainage, and intravenous antibiotics. Further diagnostic studies can be performed later, once the physician is certain that the system is sterile. This strategy prevents further clinical deterioration.

Extraureteric causes of ureteral obstruction include retroperitoneal lymphadenopathy from metastatic tumors or lymphoma, retroperitoneal fibrosis, uterine myoma, bladder masses, and high-stage pelvic tumors (eg, cervical cancer).

Anything that causes severe bladder outlet obstruction leads to bilateral hydronephrosis or hydronephrosis of a solitary kidney. Congenital anomalies can also directly obstruct or provide stasis that may lead to pyelonephritis and papillary necrosis. Duplicate collecting systems, vesicoureteral reflux, and ureteroceles are important offenders to consider.

In the clinical scenario of fever, chills, prostration, and sepsis without hydronephrosis, the differential diagnoses include pyelonephritis, perinephric abscess, renal hemorrhage, tubulointerstitial nephritis, and glomerulonephritis.

In asymptomatic patients who present with acute renal failure characterized by azotemia, the physician must consider bilateral obstruction or the presence of a solitary obstructed kidney. Renal ultrasonography is a wise first test in this scenario, along with tests for urine and plasma urea, creatinine, sodium, and osmolality. After excluding postrenal causes, consider prerenal and renal sources.

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