Nephroangiesclerosis

Nephroangiosclerosis is the involvement of the small renal vessels due to the action of arterial hypertension on them. It is an affectation that depends on the time of evolution of the hypertension and the figures, so that the higher the blood pressure, the higher the incidence of nephroangiosclerosis occurs. However, blood pressure figures do not determine the severity of the injury, but only increase the risk of it occurring.

A differentiation must be made between benign nephroangiosclerosis, which is that which occurs as a consequence of long-standing arterial hypertension and which, therefore, is also related to aging, and malignant nephroangiosclerosis, which is the involvement of the arterioles and glomeruli due to malignant arterial hypertension, poorly controlled and associated with alterations in other organs secondary to hypertension.

Malignant nephroangiosclerosis occurs in 1-5% of patients with arterial hypertension and occurs because it is no longer well controlled and becomes malignant, or due to complications secondary to hypertension and other causes, such as IgA-mediated glomerulonephritis, renal vein hypertension, systemic diseases such as scleroderma, vasculitis, the use of oral contraceptives or hemolytic uremic syndrome.

How is it produced?

In the case of benign nephroangiosclerosis, the fact that the renal arterioles have to work under increased blood pressure causes their wall to thicken, which we know as hypertrophy. Likewise, deposits of a tissue accumulate on the wall, which is produced by the injury caused to the vessel as a consequence of the high blood pressure maintained.

With respect to malignant nephroangiosclerosis, the mechanism is similar, but as the vessels are more affected, the arterioles suffer more and end up undergoing cell death, so that the dead cells are replaced by fibrous tissue. The fact of working with very high and poorly controlled blood pressure in vessels that are damaged causes their permeability to increase, so that on the one hand the filtration and purification capacity of the blood decreases, and on the other hand a substance accumulates fibrous in the vessels that makes the irrigation and, consequently, the lesion worse.

Symptoms

In the case of benign nephroangiosclerosis, these will be patients with a history of long-term arterial hypertension. In general, they are patients with other associated pathologies, such as diabetes, dyslipidaemia, obesity or elevated uric acid.

By decreasing the flow of the arterioles, a certain degree of lack of blood supply to the kidney occurs, a fact that causes an increase in diuresis, as well as the expulsion of sodium in the urine.

Kidney failure is mild and occurs in rare cases. Proteinuria, if it occurs, is usually less than 2 grams / day. Very rarely it evolves into chronic kidney failure.

In general, it is associated with vascular disorders secondary to arterial hypertension in other parts of the body, such as, for example, involvement of the vessels of the retina or enlargement of the left ventricle.

With regard to malignant nephroangiosclerosis, very high blood pressure figures will be observed, with diastolic blood pressures above 130 mm Hg, severe retinal vessel involvement secondary to arterial hypertension (occasionally papilledema may occur) and severe and progressive kidney failure.

There will be a marked proteinuria, above 3.5 g / day and microscopic hematuria; blood in urine can sometimes be seen with the naked eye.

Renal failure will condition a picture of uremia with possible neurological alterations. In turn, the same high blood pressure, probably due to cerebral edema, can give neurological symptoms that can range from headache and visual disturbances to confusion, seizures or a coma.

Associated hypertensive cardiomyopathy is frequently seen, that is, an involvement of the cardiac musculature secondary to the action of hypertension.

Diagnosis

The accurate diagnosis of nephroangiosclerosis, be it benign or malignant, would be given by a renal biopsy, but given the aggressiveness of this technique, the diagnosis will be based on the clinic and laboratory findings.

In benign nephroangiosclerosis we will see a history of long-term arterial hypertension generally associated with retinal involvement and hypertrophy of the left ventricle of the heart. A moderate proteinuria will be observed and in the analytical one a creatinine superior to 1.8 mg / dl. In order to speak properly of benign nephroangiosclerosis, there must be no primary kidney disease.

The diagnosis of malignant nephroangiosclerosis will be based on the existence of arterial hypertension with severe involvement of the retinal vessels and symptomatic renal failure. Marked proteinuria will be seen in the urine test, as well as a decrease in potassium levels and an increase in urea, creatinine and erythrocyte sedimentation rate (ESR) in the blood test. If creatinine levels are less than 2.5 mg / dl, the process may still be reversible.

Due to the involvement of the vessels, the red blood cells can break when passing through them, for which a hemolytic anemia will be observed, with the characteristic broken red blood cells (schistocytes) in the blood analysis.

Treatment

Treatment in the case of benign nephroangiosclerosis will be based on adequate control of blood pressure levels through diet and antihypertensive drugs, preferably ACEIs and ARBs. Also, other vascular risk factors, such as diabetes, obesity, cholesterol, triglycerides, and uric acid, should be controlled.

Malignant nephroangiosclerosis requires urgent correction of blood pressure levels, initially with intravenous drugs and then oral antihypertensives, such as ACE inhibitors, ARBs, beta-blockers, diuretics, and calcium antagonists. The reduction in blood pressure figures should not be abrupt, but should be done gradually over 24-48 hours so as not to compromise the kidney's blood supply.

Chronic kidney failure secondary to malignant nephroangiosclerosis should be resolved by dialysis.

Precautionary measures

It should be based on the early detection of high blood pressure and treat it through diet and drugs prescribed by the doctor. The rest of risk factors, such as cholesterol, smoking, diabetes, obesity and uric acid should also be controlled, maintaining a balanced diet, low in salt and fat, and exercising regularly.