Nephrology for the Family Physician - O.I. Bakaliuk 2003

Key Semiotics of Kidney Diseases
Acute Nephritic Syndrome

The specified syndrome includes a set of symptoms that are most characteristic of acute GN or an Exacerbation of chronic GN: sudden onset of edema, oliguria, Hypertension, and pathological urinary changes (R.B. Minkin, 1990; A.S. Chizh, 1994; T.D. Nikula, 2000). The syndrome of renal edema manifests in two variants: "nephritic" and "nephrotic". The Pathogenesis and Clinical Features of these edema variants and renal hypertension are described below. At the maximum degree of severity of acute nephritic syndrome, life-threatening complications may occur, such as acute or subacute left ventricular failure, strokes, renal Eclampsia, and ARF.

Left ventricular failure accompanied by a gallop rhythm, attacks of cardiac asthma, and pulmonary edema (3% of GN cases) holds a special place due to its unfavorable prognosis for survival, even in young patients. The specific feature of this condition is that hypervolemia resulting from acute sodium and Water retention requires the immediate intravenous administration of potent Diuretics.

The Clinical presentation of acute left ventricular failure, as well as cerebrovascular disorders, is well known; therefore, we will describe the clinical features of renal eclampsia in greater detail.

Renal eclampsia (from Greek eclampsia — flashing) refers to paroxysmal seizure activity resembling Epilepsy, which occurs most frequently in acute GN, exacerbation of chronic GN, or PE (5–8% of cases). Renal eclampsia attacks can be triggered by the consumption of salty foods or significant amounts of fluid.

In the pathogenesis of renal eclampsia, a leading role is played by increased intracranial pressure, cerebral edema, and cerebral angiospasm resulting from sodium retention in the body, as well as an increase in circulating Blood volume (CBV). According to recent data, the onset of this pathological condition is associated with excessive activation of the systemic and local RAS and overexpression of Ang II, an extremely potent pressor agent. This is accompanied by vascular spasm and an increase in peripheral vascular resistance, activation of aldosterone production, and enhanced tubular sodium reabsorption. True uremia, i.e., the retention of nitrogenous metabolic products in the body, is not observed in this case.

The classic course of a renal eclampsia attack was described back in 1924 by S.S. Zimnitsky. Its precursors include pronounced weakness, somnolence, depression, occipital headache, loss of appetite, vomiting, short-term Vision loss (amaurosis), speech difficulties, and transient paralysis. This is accompanied by a rapid increase in blood pressure and bradycardia. The first phase of renal eclampsia (A.V. Yepishin, 1998) is characterized by twitching of individual Muscle groups and the loss of pupillary Reflexes. The second phase features tonic convulsions of the skeletal Muscles with a predominance of extensor tone (opisthotonos), trismus, and mydriasis. Opisthotonos is replaced by pronounced clonic seizures (Phase III). During this phase, due to apnea, the patient's face becomes cyanotic, neck Veins distend, Tongue biting may occur, and foam (white or pinkish-white) flows from the Mouth. The eyeballs deviate or roll upward, pupils are dilated and unresponsive to light, and involuntary defecation and urination are frequently possible. In the clonic phase, breathing resumes and cyanosis diminishes. Tendon reflexes are typically enhanced, a positive Babinski sign is recorded, body Temperature rises, and fundoscopic examination reveals signs of papilledema (E.M. Tareyev, 1957; V.M. Vasyliuk, 1997; T.D. Nikula, 2000). The patient loses consciousness even before the onset of convulsions.

A renal eclampsia attack lasts from 1 to 30 minutes, tending to last longer than an epileptic seizure. In some cases, 1–3 consecutive attacks occur, after which the patient remains in a state of deep sopor or coma for some time, and upon waking, disorientation, amaurosis, and aphasia persist. In certain instances, these attacks present atypically—without loss of consciousness, twitching of individual muscle groups, or transient amaurosis and aphasia. Occasionally, death may occur due to asphyxia, Cerebral Hemorrhage, or pulmonary edema.

In 1% of cases, renal injury follows an acute pattern (anuria). In such instances, one should primarily consider The Development of rapidly progressive GN as the cause of ARF and the potential need for hemodialysis under specific conditions.