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Infectious Diseases · Zoonotic Infections — 2024 Study Guide

Clinical presentation of HFRS

Febris haemorrhagica cum syndromo renali

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral infection characterized by severe intoxication, vascular damage, and kidney injury. The clinical picture is strictly cyclic, ranging from acute fever and oliguria to profuse polyuria and prolonged recovery.

Main signAcute renal failure with decreased diuresis
Blood testThrombocytopenia, high leukocytosis, and left shift
CyclicalityOliguria is replaced by polyuria (up to 5 liters of urine per day)
Red flagTachycardia at the peak of the disease indicates myocardial damage
4 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Main clinical syndromes

HFRS manifests as systemic capillary damage, which determines the variety of complaints.

  • Pain syndrome: aching lower back pain is typical, starting on days 2–3 of fever and peaking by days 5–6. Because of this, patients assume a forced posture. Abdominal pain increases in parallel with the progression of renal impairment.
  • Hemorrhagic syndrome: manifests as petechial rash, scleral hemorrhages, and bleeding of various localizations (from epistaxis and gingival bleeding to gastrointestinal and renal bleeding). Usually, hemorrhages disappear between the 8th and 15th days.
  • Cardiovascular system: hypotension and bradycardia are characteristic at the peak of the disease. The appearance of tachycardia is a poor prognostic sign. Arterial hypertension may develop in the presence of high azotemia.
  • Nervous system and GI tract: patients suffer from severe frontotemporal headache, insomnia, «floaters» and «fog» before the eyes. Severe nausea and recurrent vomiting (up to 15–20 times a day with hiccups), dryness of the tongue, and constipation are characteristic.

Dynamics of renal syndrome

Kidney damage is the leading pathology determining the severity and outcome of HFRS. Constant markers are lower back pain and a positive Pasternatsky sign. A key diagnostic measure is strict monitoring of daily diuresis.

  1. Oliguric phase: urine output drops sharply to 300–900 ml per day, down to anuria (less than 200 ml) in severe cases. This stage lasts up to the 9th–13th day of the disease.
  2. Polyuric phase: diuresis compensatorily increases to 5 liters per day. The excretory function of the kidneys recovers in 1–2 weeks, whereas the concentrating function takes 3 to 5 weeks.
  3. Convalescence: a long period during which post-infectious asthenia persists. It is important to note that a subacute or chronic course is not characteristic of HFRS.
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Laboratory profile

Tests clearly reflect acute renal failure (ARF) and systemic inflammation.

  • Urinalysis: massive proteinuria and microhematuria are detected. A key sign is hyposthenuria (urine specific gravity remains fixed at 1001–1015). Sediment microscopy reveals casts, as well as specific Dunaevsky cells (vacuolated renal epithelium).
  • Complete blood count: pronounced leukocytosis (sometimes up to 40,000 in 1 µl) with a left shift is characteristic. The number of monocytes increases, and plasma cells appear. Thrombocytopenia is typical, the level of which correlates with the severity of the disease.
  • Blood biochemistry: classic azotemia (increased urea, creatinine, and residual nitrogen levels) against the background of hypoproteinemia.

For specific confirmation of the diagnosis, IFAT with paired sera is used — a diagnostic criterion is an increase in antibody titer by at least 4 times.

Severity assessment

The severity of HFRS is determined by the degree of ARF, intoxication, and hemorrhagic manifestations.

  • Mild course: body temperature does not exceed 38°C, intoxication is insignificant. Urea and residual nitrogen are normal, creatinine is up to 130 µmol/l.
  • Moderate course: fever up to 40°C, intense pain, visual disturbances, frequent vomiting. Hemorrhagic rash appears. Oliguria develops with moderate azotemia (creatinine up to 300 µmol/l).
  • Severe course: accompanied by infectious-toxic shock, massive bleeding, development of «acute abdomen» or DIC syndrome. Oliguria turns into anuria. Uremia develops (creatinine ≥ 300 µmol/l). Cerebral symptoms (meningeal signs, cranial nerve paresis) often join.

Briefly: answers to topical questions

What instrumental research methods are used to assess kidney function in HFRS?

Ultrasound diagnostics, excretory urography, and radioisotope radiography are used to assess kidney function in HFRS.

  • Ultrasound diagnostics — reveals enlarged kidneys, increased cortical echogenicity, and specific parenchymal edema («spared pyramids sign»).
  • Excretory urography — used when necessary as part of the examination.
  • Radioisotope radiography — performed according to indications at the dispensary follow-up stage.

Which immunoglobulin classes are determined in the serological diagnosis of HFRS?

Specific antibodies of classes M and G are determined in the serological diagnosis of HFRS.

  • IgM — class M antibodies to hantaviruses (HFRS pathogens).
  • IgG — class G antibodies to hantaviruses (HFRS pathogens).

These immunoglobulin classes are studied in the patient's blood to identify the pathogen, confirm the etiological factor, and establish the final clinical diagnosis.

What is the pathogenesis of infectious-toxic shock development in HFRS?

Microcirculation disorders underlie the pathogenesis of infectious-toxic shock (ITS) in HFRS.

  • Microcirculation disorder — leads to pronounced ischemia of organs and tissues.

The consequence of these processes is the development of ITS and multi-organ failure (acute renal, adrenal, pituitary failure, and respiratory distress syndrome). The metabolic disorders arising in this case further aggravate hemostasis disorders.

How to memorize

The rule of the «Five P's» in HFRS: P — Polyuria/Oliguria (renal), P — Pain (lower back), P — Petechiae (hemorrhagic syndrome), P — Pressure drop (hypotension), P — Proteinuria.

Class and exam questions

Is a patient with HFRS contagious to others?

No, patients do not pose an epidemiological hazard; transmission from person to person does not occur. Patients can be hospitalized in a general-profile hospital.

What are Dunaevsky cells?

These are desquamated vacuolated renal tubular epithelial cells. Their detection in urine sediment is a characteristic microscopic sign of HFRS.

Can anticoagulants be used in hemorrhagic syndrome?

Most researchers consider the use of anticoagulants (heparin, fraxiparine) in HFRS to be impractical.

Which infections should HFRS be differentiated from first?

With leptospirosis, severe influenza, typhoid fever, as well as acute pyelonephritis and surgical pathology («acute abdomen» syndrome).

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What else to study on this topic

  • Differential diagnosis of HFRS and leptospirosis
  • Life-threatening complications: ITS, pulmonary edema, and kidney rupture
  • Etiotropic therapy: ribavirin administration regimen
  • Indications for hemodialysis in HFRS
  • Long-term follow-up regimen for convalescents

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