Persistent Hypercalcemia Leading to Acute Pancreatitis in a Patient with Relapsed Myeloma and Renal Failure

Nephron ◽  
1998 ◽  
Vol 79 (1) ◽  
pp. 109-110 ◽  
Author(s):  
İsmail Çelik ◽  
Şule Apraş ◽  
Ayşe Kars ◽  
İbrahim Barışta ◽  
İbrahim Güllü ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Pancreatitis ◽  
Relapsed Myeloma

scholarly journals Acute pancreatitis : a newly recognised potential complication of canine babesiosis

2000 ◽  
Vol 71 (4) ◽  
Author(s):  
A.J. Möhr ◽  
R.G. Lobetti ◽  
J.J. Van der Lugt
Keyword(s):  
Renal Failure ◽  
Acute Pancreatitis ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Haemolytic Anaemia ◽  
Distress Syndrome ◽  
Pathophysiological Mechanism ◽  
Canine Babesiosis ◽  
Immune Mediated

This retrospective study describes 4 cases of canine babesiosis with histologically confirmed acute pancreatitis. In addition, 16 dogs with babesiosis are reported with serum amylase (>3500 U/l ) and/or lipase (>650 U/l ) activity elevations of a magnitude that would support a diagnosis of probable acute pancreatitis, although extra-pancreatic sources of the enzymes could not be excluded in these cases. Median time of pancreatitis diagnosis was 2.5 days post-admission, with primarily young (median age 3 years), sexually intact dogs affected. The development of pancreatitis was unrelated to the degree of anaemia at time of admission. In addition to pancreatitis, 80 % of cases suffered from other babesial complications, namely icterus (13), acute respiratory distress syndrome (6), immune-mediated haemolytic anaemia (6), renal failure (3), haemoconcentration (2) and cerebral syndrome (2). Acute respiratory distress syndrome, renal failure and cerebral syndrome were associated with a poor prognosis, with 4 of the 5 dogs included in the overall 26 % mortality rate having at least 1 of these complications. Haemolytic anaemia with ischaemia-reperfusion injury to the pancreas is proposed as a possible primary pathophysiological mechanism in babesial pancreatitis. Hypotensive shock, immune-mediated haemolytic anaemia, haemoconcentration and possibly altered lipid metabolism in babesiosis may also be involved. The previously postulated pro-inflammatory cytokine milieu of complicated babesiosis may underlie the progression, if not the primary initiation, of pancreatic pathology. Acute pancreatitis may represent the previously reported 'gut' form of babesiosis.

scholarly journals Atypical haemolytic uremic syndrome secondary to acute pancreatitis: a unique presentation

2019 ◽  
Vol 12 (9) ◽  
pp. e230822 ◽  
Author(s):  
Jacob Barish ◽  
Pallavi Kopparthy ◽  
Bradley Fletcher
Keyword(s):  
Renal Failure ◽  
Acute Pancreatitis ◽  
Early Recognition ◽  
Standard Of Care ◽  
Timely Manner ◽  
Haemolytic Uremic Syndrome ◽  
Complement Dysregulation ◽  
Atypical Haemolytic Uraemic Syndrome ◽  
Uremic Syndrome ◽  
To Receive

Atypical haemolytic uraemic syndrome (aHUS) is a disease of complement dysregulation and can be fatal if not treated in a timely manner. Although normally associated with triggers such as infection or pregnancy, this case demonstrates acute pancreatitis as the triggering event. The patient’s initial presentation of thrombocytopaenia and acute renal failure was first attributed to a systemic inflammatory response syndrome due to pancreatitis, but with detailed history and further laboratory investigation, we were able to show that patient was having symptoms associated with aHUS. On early recognition of aHUS, this patient was able to receive the proper standard of care with eculizumab and had a full recovery while preventing renal failure. When patients present with thrombocytopaenia and renal failure in acute pancreatitis, we want to ensure physicians keep aHUS on the differential.

Gadolinium Arteriography Complicated by Acute Pancreatitis and Acute Renal Failure

2001 ◽  
Vol 12 (3) ◽  
pp. 393 ◽  
Author(s):  
Matthew P. Schenker ◽  
Jeffrey A. Solomon ◽  
David A. Roberts
Keyword(s):  
Renal Failure ◽  
Acute Pancreatitis ◽  
Acute Renal Failure

Acute Renal Failure Complicating Severe Acute Pancreatitis

Renal Failure ◽  
1996 ◽  
Vol 18 (4) ◽  
pp. 621-628 ◽  
Author(s):  
Petar Kes ◽  
Željko VuČIČEviĆ ◽  
Iva RatkoviĆ-GusiĆ ◽  
Antun Fotivec
Keyword(s):  
Renal Failure ◽  
Acute Pancreatitis ◽  
Acute Renal Failure ◽  
Severe Acute Pancreatitis

ACUTE RENAL FAILURE IN SEVERE ACUTE PANCREATITIS (LITERATURE REVIEW)

2018 ◽  
Vol 1 ◽  
pp. 57-64
Author(s):  
O.Kh. Khalidov ◽  
◽  
D.A. Gudkov ◽  
V.S. Fomin ◽  
◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Pancreatitis ◽  
Acute Renal Failure ◽  
Literature Review ◽  
Severe Acute Pancreatitis

Renal failure in dogs with experimental acute pancreatitis: role of hypovolemia

1986 ◽  
Vol 251 (6) ◽  
pp. F969-F977 ◽  
Author(s):  
M. Levy ◽  
R. Geller ◽  
S. Hymovitch
Keyword(s):  
Renal Failure ◽  
Acute Pancreatitis ◽  
Cardiac Output ◽  
Plasma Volume ◽  
Renal Perfusion ◽  
Plasma Protein Concentration ◽  
Protein Rich ◽  
Control State ◽  
Glomerular Morphology

The factors causing a decline in renal perfusion were studied in anaesthetized dogs with acute pancreatitis 4 h after the forceful injection of bile into the pancreatic duct. In 11 such dogs, glomerular filtration rate (GFR) decreased by 40.4% from the control state (P less than 0.05), whereas the clearance of para-aminohippurate (CPAH) declined by 50.2%. These changes were associated with a 15.3% decline in cardiac output (P less than 0.05) and a 26.2% fall in plasma volume. Glomerular morphology was entirely normal. When hypovolemia was prevented by infusing homologous plasma over the 4-h period of observation, the normally observed decline in GFR, CPAH, and cardiac output was prevented. The decline in plasma volume, associated with a rising hematocrit and declining plasma protein concentration, and the associated decrement in renal perfusion, could be entirely duplicated by the infusion of trypsin, chymotrypsin, elastase, and phospholipase A2 (but not lipase or amylase) into normal dogs. These perturbations also were prevented by the concurrent infusion of 4% albumin in saline. At 24 h, however, the renal failure became unresponsive to volume replenishment. We conclude that the decline in renal perfusion in dogs at 4 h with acute pancreatitis is entirely due to hypovolemia, induced by the release of specific enzymes from the inflamed gland, which causes the loss of protein-rich plasma from the vascular space.

scholarly journals Cytomegalovirus Infection Associated with Acute Pancreatitis, Rhabdomyolysis and Renal Failure.

1992 ◽  
Vol 31 (3) ◽  
pp. 426-430 ◽  
Author(s):  
Naruhiro YASUMOTO ◽  
Mitiaki HARA ◽  
Yasunori KITAMOTO ◽  
Mahito NAKAYAMA ◽  
Tatsuo SATO
Keyword(s):  
Renal Failure ◽  
Acute Pancreatitis ◽  
Cytomegalovirus Infection

scholarly journals A Rare Case of Thrombotic Thrombocytopenic Purpura Caused by Acute Pancreatitis

2021 ◽  
Vol 51 (2) ◽  
Author(s):  
Emin Gemcioglu ◽  
Mehmet Kayaalp ◽  
Merve Caglayan ◽  
Ahmet Ceylan ◽  
Mehmet Sezgin Pepeler
Keyword(s):  
Renal Failure ◽  
Acute Pancreatitis ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Hemolytic Anemia ◽  
Neurological Disorders ◽  
Rare Case ◽  
Rare Complication ◽  
Microangiopathic Hemolytic Anemia ◽  
Peripheral Smear ◽  
Thrombocytopenic Purpura

Thrombotic Thrombocytopenic Purpura is a syndrome of microangiopathic hemolytic anemia accompanied by thrombocytopenia, neurological disorders, renal failure and fever. Acute pancreatitis is a rare cause of Thrombotic Thrombocytopenic Purpura and this manifestation, at the same time, is a rare complication of acute pancreatitis. Thrombotic Thrombocytopenic Purpura is induced in acute pancreatitis by poorly understood mechanism, which involves multiple pathways apart from only ADAMTS-13 deficiency. Here, we analyze the case of a 47-year-old female who presented with an acute pancreatitis. She was diagnosed with Thrombotic Thrombocytopenic Purpura and an acute pancreatitis at the same time, with thrombocytopenia and peripheral smear findings at presentation. Therefore, Thrombotic Thrombocytopenic Purpura secondary to the pancreatitis was considered in this case. In this work, we have discussed details of our case and the different mechanisms involved in pathogenesis of Thrombotic Thrombocytopenic Purpura in acute pancreatitis and their outcome with prompt management.

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