Renal infarction N28.0

In 1988, Pickering et al. described a syndrome in which cardiac recurrent pulmonary edema can occur due to bilateral atheromatous stenosis of the renal artery. The syndrome was named after Pickering (Messerli 2011).

Renal infarction is the sudden occlusion of the renal artery or one of the segmental arteries, leading to potential loss of function of the kidney or loss of parenchyma of the supplied segment (Engelbrecht 2017), or occlusion of a renal vein due to thrombosis, which is also called "hemorrhagic infarction" (Manski 2019).

Renal infarction is divided into anemic and hemorrhagic infarction.

Anemic infarction: This is an arterial infarction of the renal artery or its branches. A distinction is made between:

• thromboembolism (the most common form, accounting for about 90 % of cases)
• or renal artery thrombosis

Hemorrhagic infarction: a venous infarction of the renal artery or its branches (Manski 2019).

In general autopsies, anemic renal infarcts are found in up to 1.4 - 4.0 % (Remmele 2013). Healed infarcts are thus not rare, in contrast to acute renal infarcts, which account for only 0.02 of 1,000 emergency patients (Manski 2019).

The most common cause of anemic renal infarction due to thromboembolism is:

• Emboli triggered by atrial fibrillation (Herold 2021).

Less common causes may include:

• Aneurysms
• Mitral valve stenosis
• Mitral valve regurgitation
• Endocarditis
• Heart valve replacement
• Z. n. PTA (percutaneous transluminal angioplasty)
• Z. n. PTCA (percutaneous transluminal coronary angioplasty) (Manski 2019)

Cause of anemic renal infarction due to renal artery thrombosis are:

• Plaque formation in renal artery atherosclerosis (most common cause).

and more rarely:

• Renal trauma
• Vasculitis
• Iatrogenically caused (Manski 2019).
• Fat embolism
• Endocarditis (Kasper 2015)

Venous thrombosis can be caused by:

• Right heart failure
• by tumor compression (Claus 2019)
• patent foramen ovale (Kasper 2015).

Hemorrhagic infarction usually occurs in the setting of an underlying chronic disease such as:

• nephrotic syndrome
• Thrombophilia
• tumor disease
• postoperative after kidney transplantation
• is often associated with the use of oral contraceptives (Segerer 2014)

In arterial occlusions, wedge-shaped infarcts with hemorrhagic rim are found, whereas in venous occlusions, hemorrhagic infarction is present (Manski 2019).

In most cases, renal infarcts are not identified as such (Manski 2019).

Symptoms may include:

• Lumbar pain
• haematuria (Herold 2021)
• irregular pulse
• arterial hypertension (usually develops very suddenly due to the release of renin from the ischemic area [Kasper 2015])
• fever
• nausea
• vomiting
• Oliguria
• Anuria (if both kidneys are affected) (Kasper 2015 / Manski 2019).
• Venous congestion of the left-sided testis with left-sided thrombosis (Herold 2021)

Color Doppler sonography: The method of choice for renal infarction is color Doppler sonography (Herold 2021). Here, the maximum systolic flow (peak systolic velocity) is determined. This can assume flow velocities of > 260 cm / sec in higher-grade stenoses. The sensitivity of the method is 85% and the specificity 92%. In principle, the upstream iliac vessels should also be included in the examination (Risler 2008). After healing of a segmental infarct, deeply indented scars remain in the parenchyma. In the case of a complete infarction, a shrunken kidney forms (Manski 2019).

Contrast CT: Renal infarction can also be detected by contrast CT if there is no renal insufficiency or other contraindications (Seeler 2005).

In anemic infarction, it is recommended to investigate the cause:

• Resting ECG
• Long-term ECG
• Event recorder
• Abdominal sonography with tumor search (Claus 2019)

• Hematuria
• Proteinuria
• GOT (usually only slightly elevated)
• AP (also only slightly elevated)

[Herold 2021)

And as a sign of cellular decay [Manski 2019])

• LDL (can rise to extreme levels [Kasper 2015]
• CK
• Creatinine increase
• Cystatin C increase [Manski 2019].

• Hematuria
• Proteinuria
• GOT (usually only slightly elevated)
• AP (also only slightly elevated) (Herold 2021)

And as a sign of cellular decay [Manski 2019])

• LDL (can rise to extreme levels [Kasper 2015]
• CK
• Creatinine increase
• Cystatin C increase [Manski 2019].

Anemic renal infarction is typically cone-shaped with the base directed toward the renal capsule and the tip extending into the medulla. The narrow cortex-parenchyma border remains vital due to the preserved blood supply through capsular vessels.

The infarcted area collapses after approximately one week and is transformed into a scarred structure over several weeks.

(Thomas 2006)

• acute renal failure (however, this occurs only very rarely [Segerer 2014])
• arterial hypertension (occurs a few days after renal infarction [Herold 2021])
• pulmonary oedema (may occur in bilateral stenosis of the renal arteries [Messerli 2011])

Renal infarction can be treated conservatively with:

• Analgesics
• control of arterial hypertension s. d.
• systemic full heparinization

Lysis therapy should be decided depending on the extent of the infarction and the remaining renal function (Manski 2019).

If the diagnosis is made in time, anatomical or extraanatomical bypass surgery is available.

Bypass measures are indicated for:

• single kidney
• bilateral embolism

The time window for these surgical measures is not clearly defined (Manski 2019).

If only one kidney is affected, the effects on renal function are often minor. After the ischemic tissue has transformed into scar tissue, the arterial hypertension can regress due to the reduced release of renin (Kasper 2015).

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