Renal papillary necrosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

Renal papillary necrosis is a form of nephropathy involving the ischemic necrosis of the renal papilla, which is supplied by the vasa recta. Renal papillary necrosis is a significant kidney disorder, which is associated with chronic conditions such as diabetes, sickle cell disease, urinary tract obstruction, urinary tract infection and long term use of analgesics containing phenacetin.

Renal papillary necrosis was first introduced by Friedrich in 1877, following urinary obstruction. Then, other associated factors such as diabetes, sickle cell disease and analgesics have been found.

It is thought that Renal papillary necrosis is the result of damage to interstitial medullary and papillary cells due to direct effect of diseases such as diabetes, sickle cell disease, urinary tract obstruction, renal vein thrombosis, upper urinary tract infection, tuberculosis, vasculitis, renal transplant rejection and long term analgesics use such as acetaminophen and NSAIDs. Decreased prostaglandin synthesis and subsequent reduced renal blood flow is an important mechanism for developing renal papillary necrosis. Accumulation of sickle-shaped RBCs in patients with sickle cell disease can lead to intravascular obstruction, blood stasis and thrombosis that results in ischemic necrosis of renal papillary and medullary cells.

Renal papillary necrosis is associated with damaging the renal medullary and papillary cells due to many diseases such as diabetes, sickle cell disease, urinary tract obstruction, renal vein thrombosis, pyelonephritis, tuberculosis, vasculitis, cirrhosis, renal transplant rejection and long term analgesics and alcohol abuse. In infants, it is associated with asphyxia, dehydration, and sepsis.

Renal papillary necrosis may be classified according to the severity of renal parenchymal lesions into two subtypes: Medullary and Papillary.

Renal papillary necrosis should be differentiated from other conditions presenting with acute flank or upper abdominal pain, hematuria, nausea and vomiting. The differentials include: nephrolithiasis, pyelonephritis, renal infarct, renal cell carcinoma, pelvic inflammatory disease, ovarian torsion, testicular torsion, prostatitis, prostatic cancer, ectopic pregnancy, orchitis, appendicitis, cholecystitis, ischemic colitis, peptic ulcer disease, portal vein thrombosis, diverticulitis, abdominal aortic aneurysm.

The prevalence and demographic characteristics of renal papillary necrosis depend on the causative agent.*Renal papillary necrosis due to analgesic abuse is more prevalent in Australia and England and less in the US. The prevalence of renal papillary necrosis was reported 65,000 per 100,000 patients with sickle cell disease.In developing countries, the incidence of renal papillary necrosis is 3900 per 100,000 persons.The prevalence of renal papillary necrosis increases with age. It commonly affects the elderly (>60 years).Renal papillary necrosis due to sickle cell disease commonly affects adults in the third and fourth decades.Renal papillary necrosis is more prevalent in women.

Common complications of renal papillary necrosis include Kidney infection and stones, chronic renal failure, kidney cancers, hypertension, anemia and ESRD. Prognosis depends on the underlying condition.

The diagnosis of renal papillary necrosis is made by a history of having high-risk conditions such as analgesic abuse and urinalysis and Ultrasound, CT, or other imaging tests of the kidneys.

The most common symptoms of renal papillary necrosis include back pain, fever, bloody urine, presence of tissues in urine, Cloudy urine, dysuria, frequency, urgency and urinary incontinency. History of medical conditions such as diabetes and sickle cell disease and long term analgesics use such as acetaminophen and NSAIDS should be considered. If left untreated or progressed, symptoms of chronic renal failure may be developed.

Common physical examination findings of renal papillary necrosis include fever, costovertebral angle tenderness, and hematuria.

CT urography is helpful in the diagnosis of renal papillary necrosis that shows multiple small accumulations of contrast media in the papillary regions near the calyx system. The lobster claw sign is a diagnostic finding on CT urography in the papillary subtype of renal papillary necrosis that develops due to elongation of the minor calyx fornices following ischemia and destruction of the renal papilla.

MRI can be used as a helpful alternative imaging test in children suspected renal papillary necrosis. On Magnetic resonance urography, renal papillary necrosis is characterized by classic signs of papillary necrosis including candle-flame appearance, Golf ball on a tee sign, lobster claw sign and clubbing of calyces.

On renal biopsy, renal papillary necrosis is characterized by necrosis of papilla, swelling and sloughing of papilla, mild inflammation and microcalcification at necrotic area.

The mainstay of therapy in renal papillary necrosis is supportive care and treating the underlying cause such as discontinuation of analgesics. In severe cases, dialysis or renal replacement therapy may be required.

The mainstay of therapy is supportive care and treating the underlying cause.

In severe cases of renal papillary necrosis leading to chronic kidney disease, dialysis or renal replacement therapy may be required.

Effective measures for the primary prevention of renal papillary necrosis include controlling underlying diseases such as diabetes or sickle cell anemia, avoid taking over-the-counter analgesics and using the minimum dose of NSAIDs within the shortest time.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

Renal papillary necrosis was first introduced by Friedrich in 1877, following urinary obstruction. Then, other associated factors such as diabetes, sickle cell disease and analgesics were found.

• Renal papillary necrosis was first discovered by professor Friedrich in 1877, in a patient following urinary obstruction due to prostatic hyperplasia. ^[1]
• Gunther and Edmonson found association between RPN and diabetes mellitus. ^[2]

• Analgesic nephropathy was first described by Spuhler and Zollinger in 1953 due to chronic use of pain killer medications containing phenacetin. ^[3]
• The association between RPN and sickle cell disease was found by Sydenstricker in 1923. ^[2]

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Renal papillary necrosis may be classified according to the severity of renal parenchymal lesions into two subtypes: Medullary and Papillary.

• Renal papillary necrosis may be classified according to the severity of renal parenchymal lesions into two subtypes^[1]:
  • Medullary
    • focal necrotic areas, without fornices involvement
  • Papillary
    • involvement of the whole calyceal systems and papillary areas

• According to the histological finding of renal papillary necrosis, there are five grades based on the severity. “Renal Papillary Necrosis – an overview | ScienceDirect Topics”.
  • Grade 1
    • involvement of microvasculature, loop of Henle, and interstitial cells, which replaced by eosinophilic material
    • intact collecting ducts
  • Grade 2
    • necrosis of apex of the papilla
  • Grade 3
    • necrosis that extends to mid-papilla
  • Grade 4
    • necrosis that extends to base of the papilla
  • Grade 5
    • necrosis that extends to the extra-medullary area

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

Renal papillary necrosis is a significant kidney disorder, which is associated with ischemia of the inner renal medulla and papilla due to chronic conditions such as diabetes, sickle cell disease, urinary tract obstruction, urinary tract infection and long term use of analgesics. Decreased prostaglandin synthesis and subsequent reduced renal blood flow is an important mechanism for developing renal papillary necrosis.

• The exact pathogenesis of renal papillary necrosis is not fully understood.
• It is thought that Renal papillary necrosis is the result of damage to interstitial medullary and papillary cells due to direct effect of diseases such as diabetes, sickle cell disease, urinary tract obstruction, renal vein thrombosis, upper urinary tract infection, tuberculosis, vasculitis, renal transplant rejection and long term analgesics use such as acetaminophen and NSAIDS. ^[1][2][3]

• Renal medullary and papillary cells are susceptible to ischemia. ^[5]
• Medullary cells usually produce prostaglandins and proteoglycans. ^[1]
  • Damage of medullary cells leads to changes in renal matrix and vessels due to decreased production of prostaglandins that causes vasoconstriction, reduced renal perfusion, ischemia and necrosis. ^[1][6]
• Another mechanism is inhibiting cyclooxygenase enzymes; COX I and COX II, which play a major role in the prostaglandins synthesis, following NSAIDS use. ^[7]
  • Multiple NSAIDS taking and hypovolemic condition could facilitate development of renal papillary necrosis. ^{[1] [2]}

• Accumulation of sickle-shaped RBCs in patients with sickle cell disease can lead to intravascular obstruction, blood stasis and thrombosis that results in ischemic necrosis of renal papillary and medullary cells.^[8]

• The most important characteristics of renal papillary necrosis on gross pathology are irregular round shaped necrosis of renal papillary and medullary area. ^{[9] [3]}

• On microscopic histopathological analysis, the characteristic findings of renal papillary necrosis include^[9][10][11]:
  • Coagulative necrosis of papillary area
  • swelling and sloughing of papilla
  • partial necrosis of medullary area
  • mild inflammation at necrotic area
  • microcalcifications at necrotic area
• Other renal histological findings include^[9][12]:
  • diabetic nephropathy:
    • diffuse nodular mesangial sclerosis
  • analgesic nephropathy:
    • interstitial fibrosis
    • cytoplasmic edema
    • dilation of organelles
    • increased production of proteoglycan
    • tubular atrophy
    • endothelial cell injury
      • capillary sclerosis
    • damage to loops of Henle
    • Platelet thrombus
  • sickle cell nephropathy:
    • intravascular obstruction
    • intravascular thrombosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

• Renal papillary necrosis is associated with damaging the renal medullary and papillary cells due to many diseases such as diabetes, sickle cell disease, urinary tract obstruction, renal vein thrombosis, pyelonephritis, tuberculosis, vasculitis, cirrhosis, renal transplant rejection and long term analgesics and alcohol abuse. In infants, it is associated with asphyxia, dehydration, and sepsis.

• Common causes of renal papillary necrosis include^[1][2][3]:
  • Diabetes
  • Sickle cell disease: most common cause in children
  • Urinary tract obstruction
  • Renal vein thrombosis
  • upper urinary tract infection or pyelonephritis
  • Tuberculosis
  • liver cirrhosis
  • systemic vasculitis
  • Renal transplant rejection
  • chronic alcohol abuse
  • abuse of acetaminophen and analgesics containing phenacetin such as NSAIDs
    • NSAIDs include:
      • Aspirin
      • Ibuprofen
      • Mefenamic acid
      • Indomethacin
      • Naproxen
      • Meloxicam
      • Diclofenac
      • Piroxicam
      • ketorolac
  • Renal papillary necrosis may also occur less commonly in infants due to^[4]:
    • asphyxia
    • dehydration
    • sepsis

• There is a mnemonic for the causes of renal papillary necrosis^[5] : POSTCARDS:
  • Pyelonephritis
  • Obstruction of the urogenital tract
  • Sickle cell disease
  • Tuberculosis
  • Cirrhosis
  • Analgesia/Alcohol abuse
  • Renal vein thrombosis
  • Diabetes mellitus
  • Systemic vasculitis

[[Category:Disease]

Renal papillary necrosis should be differentiated from other conditions presenting with acute flank or upper abdominal pain, hematuria, nausea and vomiting. The differentials include the following:^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34]}

[[Category:Disease]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

The prevalence and demographic characteristics of renal papillary necrosis depend on the causative agent.

• Renal papillary necrosis due to analgesic abuse is more prevalent in Australia and England and less in the US. ^[1]
  
  • In Australia, the prevalence of renal papillary necrosis ranges from 15000 per 100,000 persons to 20000 per 100,000 persons requiring kidney transplant. ^[1]

• The prevalence of renal papillary necrosis was reported 65,000 per 100,000 patients with sickle cell disease. ^[2]
• In Africa, the prevalence of symptomatic renal papillary necrosis was reported 2300 per 100,000 patients with sickle cell disease with homozygous S. ^[3]

• In developing countries, the incidence of renal papillary necrosis is 3900 per 100,000 persons.^[4]
• The incidence of renal papillary necrosis is 30,000 to 40,000 per 100,000 patients with Sickle cell disease. ^[5]

• The prevalence of renal papillary necrosis increases with age. It commonly affects the elderly (>60 years). “Renal Papillary Necrosis – American Urological Association”.

• Renal papillary necrosis due to sickle cell disease commonly affects adults in the third and fourth decades.^[6]

• Renal papillary necrosis is more prevalent in women.^[1][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

The most potent risk factor in the development of renal papillary necrosis is analgesics abuse. Other risk factors include pyelonephritis, diabetes, renal transplant rejection, sickle cell disease, urinary tract obstruction, cirrhosis, dehydration, hypotensive shock and hypoxia.

• The most potent risk factor in the development of renal papillary necrosis is analgesics abuse. Other risk factors include pyelonephritis, diabetes, renal transplant rejection, sickle cell disease, urinary tract obstruction, cirrhosis, dehydration, hypotensive shock and hypoxia. ^[1][2]

[[Category:Disease]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

Common complications of renal papillary necrosis include Kidney infection and stones, chronic renal failure, kidney cancers, hypertension, anemia and ESRD. Prognosis depends on the underlying condition.

• Renal papillary necrosis is associated with damage of the renal papilla due to systemic diseases and analgesics abuse. ^[1]

• Common complications of renal papillary necrosis include^[1] “Renal Papillary Necrosis – an overview | ScienceDirect Topics”.:
  • Chronic renal failure
  • Kidney infection
  • Nephrolithiasis
  • Hypertension
  • Anemia
  • End stage renal disease (ESRD)
  • Kidney cancers

• The prognosis of renal papillary necrosis depends on the underlying condition.