Symptoms of kidney damage with nodular periarteritis

Symptoms of nodular polyarteritis are distinguished by significant polymorphism. The disease, as a rule, begins gradually. An acute onset is characteristic of nodular polyarteritis of drug origin. Nodular periarteritis debuts with nonspecific symptoms: fever, myalgia, arthralgia, weight loss. The fever is of the wrong type, it does not stop when treated with antibacterial drugs and can last from several weeks to 3-4 months. Myalgia, a symptom of ischemic muscle damage, often appears in the calf muscles. Articular syndrome develops in more than half of patients with nodular polyarteritis, combining, as a rule, with myalgia. Most patients are concerned about arthralgia of large joints of the lower limbs; a small number of patients described transient arthritis. The loss of body mass observed in the majority of patients and reaching in some cases the degree of cachexia not only serves as an important diagnostic sign of the disease, but also indicates its high activity. Skin lesion in patients with generalized nodular polyarteritis is noted in the form of typical nodules (which are currently observed less frequently), located along the vessels and representing aneurysms of the subcutaneous arteries, hemorrhagic purpura, ischemic gangrene of the fingers and feet.

The common symptoms of nodular polyarteritis persist for several weeks, during which visceral lesions gradually develop.

• Abdominal syndrome is an important diagnostic and prognostic clinical sign of nodular polyarteritis, which is noted in 36-44% of patients. The syndrome manifests itself in abdominal pain of varying intensity, dyspepsia (nausea, vomiting, anorexia), diarrhea, symptoms of gastrointestinal bleeding. The cause of abdominal syndrome is ischemic damage to the abdominal organs with the development of infarcts, ischemic ulcers, perforation due to vasculitis of the corresponding vessels. With nodular polyarteritis, the small intestine is more often affected, more rarely - the large intestine and stomach. Often develop damage to the liver, gallbladder, pancreas.
• The defeat of the peripheral nervous system occurs in 50-60% of patients and manifests as asymmetric polyneuritis, the development of which is associated with ischemia of nerves as a result of involvement in the pathological process of vasa nervorum. In addition to intense pain in the limbs, sensitivity disorders, polyneuritis is accompanied by motor disorders, muscular atrophy, paresis of the feet and brushes. CNS with nodular polyarteritis is much less likely to be affected by the peripheral nervous system. Ischemic and hemorrhagic strokes, episindrom, psychiatric disorders are described.
• Defeat of the heart is noted in 40-50% of patients, and it is based on the vasculitis of the coronary arteries, which proceeds, as a rule, asymptomatically or with an atypical pain syndrome. The diagnosis of coronary artery disease is based on changes in electrocardiography (ECG). In a small percentage of cases, it is possible to develop a small-focal myocardial infarction. When lesions of small branches of the coronary arteries develop violations of rhythm and conductivity, rapidly increasing circulatory failure due to diffuse ischemic damage to the myocardium. Heart failure can also lead to severe arterial hypertension.
• Lung inflammation develops relatively rarely with classic nodular polyarteritis (no more than 15% of patients) and is associated mainly with the development of pulmonary vasculitis, less often interstitial fibrosis.
• With nodular polyarteritis, the endocrine system can be affected. Often develop orchitis or epididymitis. Defects of the thyroid gland, adrenal glands, and pituitary gland are described.
• Eye damage is noted in patients rarely and is manifested by conjunctivitis, uveitis, episcleritis. The most severe form of eye damage is the vasculitis of the central artery of the retina, leading to its occlusion and blindness.

Symptoms of nodular polyarteritis and kidney damage appear after 3-6 months from the onset of the disease. The main sign of kidney damage is hypertension, which, according to various sources, is detected in 33-80% of patients. The main pathogenetic mechanism of arterial hypertension is activation of RAAS due to kidney ischemia, which is confirmed by the presence of hypercellularity of the juxtaglomerular apparatus. In most cases, severe arterial hypertension develops with high diastolic blood pressure (300 / 180-280 / 160 mmHg), often malignant, with the development of retinopathy and edema of optic discs, acute left ventricular failure, hypertensive encephalopathy. Early severe arterial hypertension, which tends to rapid progression, usually indicates a high activity of vasculitis. However, there is no direct correlation between the severity of morphological changes and arterial hypertension, and the latter can develop after the elimination of the acute process. A feature of arterial hypertension in nodular polyarteritis is its resistance. Only 5-7% of patients have normal arterial blood pressure after reaching remission.

Impaired renal function as a moderate increase in creatinine in the blood and / or reduce glomerular filtration is noted in almost 75% of patients, but 25% of patients with kidney damage are diagnosed with severe renal failure. Oliguric acute renal failure can develop due to vascular accidents, in rare cases complicating severe vasculitis (rupture of the aneurysm of the renal artery, acute thrombosis of the kidney vessels with necrosis of the cortical substance of the kidneys).

The urinary syndrome in most cases is manifested by moderate proteinuria, not exceeding 1 g / day, and microhematuria. Massive proteinuria, reaching 6-8 g / day, is noted for malignant hypertension, but nephrotic syndrome develops in no more than 10% of patients. Macrogematuria with nodular polyarteritis develops rarely and suggests the development of a kidney infarction even without a characteristic pain syndrome or necrotizing glomerulonephritis. Rapidly progressive glomerulonephritis should be suspected in the presence of nephrotic syndrome and rapidly growing renal failure, since patients with ischemic renal damage are characterized by a stable course of chronic renal failure.

[1], [2], [3], [4]