Kidney infarction
As renal infarction in the narrow sense of the most by is embolic occlusion of a small renal artery induced destruction of kidney tissue referred to, wherein the wedge-shaped generally concerned district as so-called "white" or ischemic infarction rests with its base the renal capsule. In a broader sense, hemorrhagic infarction of the kidney caused by venous occlusion is also included.
causes
90 percent of kidney infarcts are caused by embolism , with an aortic or mitral vitium , endocarditis or cardiac wall thrombosis being the source of the embolism; Thrombotic occlusions are found in blunt abdominal trauma , arteriosclerosis , vasculitis , thrombotic microangiopathies or periarteritis . Other iatrogenic causes include the accidental ligature of a kidney vessel during surgery or infarction during angiography or angioplasty .
The decisive factor is whether the arterial vascular occlusion is complete or incomplete: Only the complete occlusion of a vessel leads to absolute ischemia with complete destruction of the kidney tissue, a subsequent resorbing inflammation and subsequent cicatricial transformation.
The incomplete closure of an arterial vessel leads to a mostly local reduced blood flow and supply of the tissue and a sub-infarction with atrophy of the renal tubules and preserved glomerules .
A hemorrhagic kidney infarction is usually the result of a circulatory shock or right heart failure with slowing of the blood flow and a thrombosis of the renal vein.
morphology
The affected tissue in acute ischemic kidney infarction has a pale yellowish color and is surrounded by a hemorrhagic border. Multiple kidney infarcts with multiple arterial occlusions of smaller renal vessels lead to a hunched appearance of the kidney, the retractions being caused by the scarred, shrunken infarct areas. When the renal artery is occluded as a central vessel, the kidney is smoothly atrophied .
In hemorrhagic kidney infarction, the kidneys (usually in their entirety) are enlarged to match the venous congestion and are dark blue-red in color.
Incidence
Since a good tenth of the cardiac output is supplied to the individual kidneys , embolic events are quite common. About four percent of all autopsies diagnose a kidney infarction (mostly silent and therefore clinically undiagnosed).
Conversely, renal artery stenosis (with renal infarction as the cause) is responsible for renal hypertension for a good 1% of all acute hypertension cases.
Symptoms
Clinically, minor kidney infarctions are often silent. Larger infarcts can be accompanied by acute, persistent and sharp flank pain which, despite its persistence, can be misinterpreted as renal colic. Fever is possible. Hematuria ( micro- or macrohematuria ), leukocytosis, and increased lactate dehydrogenase and transaminases can occur in the laboratory . If the affected kidney is a single functional kidney or if both kidneys are affected, acute kidney failure occurs .
therapy
Kidney infarcts are usually treated (conservatively) without surgery: Painkillers, regulation of blood pressure and systemic complete heparinization are the first therapeutic measures. Depending on the extent of the infarct, lysis therapy to dissolve the embolus or an emergency operation should be considered. Prerequisite for this is a timely diagnosis.
Individual evidence
- ↑ Histopathology Course, Cytopathology Course: Acute Kidney Infarction
- ↑ D. Manski: Renal artery embolism - renal infarction. on: urologielehrbuch.de