Specifically variants in G1 and G2 of apolipoprotein L1 in the African American have shown increased risk of albuminuria, and hyperfiltration. Environmental
Risk factors for papillary necrosis include analgesics, concomitant cirrhosis, diabetes, pyelonephritis, systemic vasculitis, renal vein thrombosis, and urinary tract obstruction. Diagnosis
Diagnosis is done through the exclusion of other potential causes. These include acute tubular necrosis from chronic ischemia, membranoproliferative glomerulonephropathy from hepatitis C, nephrolithiasis causing obstructive nephropathy, and papillary necrosis which could be caused by pyelonephritis, diabetes mellitus, or from NSAIDs. The use of renal biopsy is not necessary unless there is a sudden onset of large protein excretions or signs of rapidly declining renal function. Urinalysis, microalbumin to creatinine ratio, quantification of urine protein and ultrasound (to exclude obstructive nephropathy and detect papillary necrosis) are methods used to determine renal function. Early signs include abnormally large and distended glomeruli causing hyperfiltration from as young as two years old. Albuminuria has been used for initial diagnosis in children from as young as four years old but significant damage may have already occurred by the time albuminuria has been detected. Creatinine measurements may not always be accurate because while the glomerulus completely filters creatinine, secondary secretion in the proximal tubules is maximally utilized in those with SCD so GFR may appear to be higher than what it actually is. If exhibiting hematuria, a CT scan should be done to exclude medullary carcinoma and due to multiple blood transfusions, serologies of the autoantibody and complement levels of HIV, hepatitis B and C should also be done.
Most patients are between the ages of 30 and 50 years, although it has been reported in infants aged as young as 3 weeks, as well as in older people Hyperemesis gravidarum, which is severe morning sickness associated with vomiting and retching in pregnancy, is also a known cause of Mallory–Weiss tear. Diagnosis
Definitive diagnosis is by endoscopy. Proper history taking by the medical doctor to distinguish other conditions that cause haematemesis but definitive diagnosis is by conducting esophagogastroduodenoscopy. Treatment
Treatment is usually supportive as persistent bleeding is uncommon. However cauterization or injection of epinephrine to stop the bleeding may be undertaken during the index endoscopy procedure. Very rarely embolization of the arteries supplying the region may be required to stop the bleeding. If all other methods fail, high gastrostomy can be used to ligate the bleeding vessel. A Blakemore tube will not be able to stop bleeding as here the bleeding is arterial and the pressure in the balloon is not sufficient to overcome the arterial pressure. History
The condition was first described in 1929 by G. Kenneth Mallory and Soma Weiss in 15 alcoholic patients. See also
Boerhaave syndrome – Full thickness esophageal ruptures are also often secondary to vomiting/retching. Hematemesis

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