Symptoms of kidney damage in periarteritis nodosa

Symptoms of polyarteritis nodosa are characterized by significant polymorphism. The disease usually begins gradually. Acute onset is typical for drug-induced polyarteritis nodosa. Nodular periarteritis debuts with nonspecific symptoms: fever, myalgia, arthralgia, weight loss. Fever is of an irregular type, is not relieved by treatment with antibacterial drugs and can last from several weeks to 3-4 months. Myalgia, which is a symptom of ischemic muscle damage, most often appears in the calf muscles. Joint syndrome develops in more than half of patients with polyarteritis nodosa, usually combined with myalgia. Most often, patients are bothered by arthralgia of large joints of the lower extremities; transient arthritis is described in a small number of patients. Weight loss, observed in most patients and reaching the degree of cachexia in some cases, not only serves as an important diagnostic sign of the disease, but also indicates its high activity. Skin lesions in patients with generalized nodular polyarteritis are noted in the form of typical nodules (which are currently observed less and less frequently) located along the course of the vessels and representing aneurysms of the subcutaneous arteries, hemorrhagic purpura, ischemic gangrene of the fingers and toes.

General symptoms of polyarteritis nodosa persist for several weeks, during which visceral lesions gradually develop.

• Abdominal syndrome is an important diagnostic and prognostic clinical sign of polyarteritis nodosa, which is observed in 36-44% of patients. The syndrome is manifested by abdominal pain of varying intensity, dyspepsia (nausea, vomiting, anorexia), diarrhea, and symptoms of gastrointestinal bleeding. The cause of abdominal syndrome is ischemic damage to the abdominal organs with the development of infarctions, ischemic ulcers, and perforation due to vasculitis of the corresponding vessels. With polyarteritis nodosa, the small intestine is most often affected, less often the large intestine and stomach. Damage to the liver, gallbladder, and pancreas often develops.
• Peripheral nervous system damage occurs in 50-60% of patients and is manifested by asymmetric polyneuritis, the development of which is associated with nerve ischemia as a result of involvement of vasa nervorum in the pathological process. In addition to intense pain in the limbs, sensitivity disorders, polyneuritis is accompanied by movement disorders, muscle atrophy, paresis of the feet and hands. The central nervous system is affected much less frequently in nodular polyarteritis than the peripheral nervous system. Ischemic and hemorrhagic strokes, epilepsy syndrome, mental disorders have been described.
• Heart damage is observed in 40-50% of patients, and it is based on vasculitis of the coronary arteries, which is usually asymptomatic or has an atypical pain syndrome. The diagnosis of coronariitis is based on changes in electrocardiography (ECG). In a small percentage of cases, small-focal myocardial infarction may develop. When small branches of the coronary arteries are affected, rhythm and conduction disturbances develop, and circulatory failure rapidly increases due to diffuse ischemic damage to the myocardium. Severe arterial hypertension can also lead to heart failure.
• Lung damage develops relatively rarely in the classical form of polyarteritis nodosa (in no more than 15% of patients) and is associated mainly with the development of pulmonary vasculitis, less often - interstitial fibrosis.
• With nodular polyarteritis, damage to the endocrine system is possible. Orchitis or epididymitis develops more often. Damage to the thyroid gland, adrenal glands, and pituitary gland has been described.
• Eye damage is rarely observed in patients and manifests itself as conjunctivitis, uveitis, episcleritis. The most severe form of eye damage is vasculitis of the central retinal artery, leading to its occlusion and blindness.

Symptoms of polyarteritis nodosa and kidney damage appear 3-6 months after the onset of the disease. The main sign of kidney damage is arterial hypertension, detected, according to various data, in 33-80% of patients. The main pathogenetic mechanism of arterial hypertension is the activation of RAAS due to renal ischemia, which is confirmed by the presence of hypercellularity of the juxtaglomerular apparatus. In most cases, severe arterial hypertension with high diastolic blood pressure (300/180-280/160 mm Hg) develops, often malignant, with the development of retinopathy and edema of the optic nerve discs, acute left ventricular failure, hypertensive encephalopathy. Early severe arterial hypertension, which tends to progress rapidly, usually indicates high activity of vasculitis. However, there is no direct correlation between the severity of morphological changes and arterial hypertension, and the latter may develop after the acute process has been eliminated. A feature of arterial hypertension in nodular polyarteritis is its persistence. Only in 5-7% of patients does arterial pressure normalize after achieving remission.

Impaired renal function in the form of a moderate increase in blood creatinine concentration and/or decreased glomerular filtration is observed in almost 75% of patients, but severe renal failure is detected in 25% of patients with kidney damage. Oliguric acute renal failure may develop as a result of vascular catastrophes, rarely complicating severe vasculitis (renal artery aneurysm rupture, acute thrombosis of intrarenal vessels with necrosis of the renal cortex).

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 in malignant arterial hypertension, but nephrotic syndrome develops in no more than 10% of patients. Macrohematuria in nodular polyarteritis develops rarely and allows one to assume the development of renal infarction even without the characteristic pain syndrome or necrotizing glomerulonephritis. Rapidly progressive glomerulonephritis should be suspected in the presence of nephrotic syndrome and rapidly increasing renal failure, since patients with ischemic kidney damage are characterized by a stable course of chronic renal failure.

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