Alcohol is the single most common cause of chronic pancreatitis. Triglyceride levels greater than 1000 mg/dL (11.29 mmol/L) is another cause. Medications
There are seven classes of medications associated with acute pancreatitis: statins, ACE inhibitors, oral contraceptives/hormone replacement therapy (HRT), diuretics, antiretroviral therapy, valproic acid, and oral hypoglycemic agents. Mechanisms of these drugs causing pancreatitis are not known exactly, but it is possible that statins have direct toxic effect on the pancreas or through the long-term accumulation of toxic metabolites. Meanwhile, ACE inhibitors cause angioedema of the pancreas through the accumulation of bradykinin. Birth control pills and HRT cause arterial thrombosis of the pancreas through the accumulation of fat (hypertriglyceridemia). Diuretics such as furosemide have a direct toxic effect on the pancreas. Meanwhile, thiazide diuretics cause hypertriglyceridemia and hypercalcemia, where the latter is the risk factor for pancreatic stones.HIV infection itself can cause a person to be more likely to get pancreatitis. Meanwhile, antiretroviral drugs may cause metabolic disturbances such as hyperglycemia and hypercholesterolemia, which predisposes to pancreatitis. Valproic acid may have direct toxic effect on the pancreas. There are various oral hypoglycemic agents that contributes to pancreatitis including metformin. But, glucagon-like peptide-1 (GLP-1) is more strongly associated with pancreatitis by promoting inflammation.Atypical antipsychotics such as clozapine, risperidone, and olanzapine can also cause pancreatitis. Infection
A number of infectious agents have been recognized as causes of pancreatitis including:
Viruses
Coxsackie virus
Cytomegalovirus
Hepatitis B
Herpes simplex virus
Mumps
Varicella-zoster virus
Bacteria
Legionella
Leptospira
Mycoplasma
Salmonella
Fungi
Aspergillus
Parasites
Ascaris
Cryptosporidium
Toxoplasma

Other
Other common causes include trauma, autoimmune disease, high blood calcium, hypothermia, and endoscopic retrograde cholangiopancreatography (ERCP).
Some mutations in genes associated with renal dysplasia (in syndromes) have been determined. The mutations in question occur at EYA1 or SIX1 genes (branchio-oto-renal syndrome). The PAX2 gene is also thought to play a role in MCDK.The contralateral kidney often undergoes hypertrophy. This is believed to be a compensatory mechanism to the non-functional MCDK. About 90% of patients with an MCDK will have contralateral hypertrophy into adulthood. The impact of contralateral hypertrophy on long-term renal outcomes is unknown. Diagnosis
MCDK is usually diagnosed by ultrasound examination before birth. Mean age at the time of antenatal diagnosis is about 28 weeks A microscopic analysis of urine in individuals with probable multicystic dysplastic kidney should be done. One meta-analysis demonstrated that unilateral MCDK occurs more frequently in males and the greater percentage of MCKD occur on the left side of the body. Treatment
MCDK is not treatable. However, the patient is observed periodically for the first few years during which ultrasounds are generally taken to ensure the healthy kidney is functioning properly and that the unhealthy kidney is not causing adverse effects. In severe cases MCDK can lead to neonatal fatality (in bilateral cases), however in unilateral cases the prognosis might be better (it would be dependent on associated anomalies). Epidemiology
In regard to the epidemiology of multicystic dysplasia kidney, the incidence of MCDK is estimated to be 1 in every 4,000 live births, making it rare in terms of the general population. References
Further reading
Al-Khaldi, N.; Watson, A. R.; Zuccollo, J.; Twining, P.; Rose, D. H. (1994).