Evolution of concepts of the disease
Richard Bright is considered the founder of modern nephrology, having described the classic clinical presentation of kidney damage over 150 years ago. Bright's triad includes:
- Changes in the patient's appearance (characteristic pallor of the skin, in which "the healthy complexion fades").
- Subjective manifestations (pain in the lumbar region, progressive general weakness, dyspeptic disorders up to vomiting, and depressed mood).
- Laboratory marker — the appearance of protein in the urine (albuminuria).
A huge contribution to the study of the pathology was made by the Soviet school, in particular E. M. Tareev, who published the monograph "Anemia of Bright's Disease Patients" in 1929. The main methodological principle of his school was the priority of careful physical examination at the patient's bedside over instrumental diagnostics. Tareev warned doctors against an excessive passion for complex equipment to the detriment of clinical thinking.
Today, as Tareev foresaw, nephrologists face new challenges: the frequent involvement of the kidneys in systemic pathological processes, the connection of nephropathies with viral infections, and the rapid growth of drug-induced (nephrotoxic) injuries.
Metabolic and trophic disorders
Decreased renal function inevitably triggers a cascade of severe metabolic disorders throughout the body:
- Protein metabolism: the development of hypoproteinemia leads to a pronounced decrease in muscle mass and patient exhaustion.
- Lipid metabolism: against the background of hyperlipidemia, atherosclerotic changes in blood vessels are accelerated.
- Mineral metabolism: calcium metabolism is disrupted, and a persistent deficiency of vital trace elements — zinc, copper, and iron — occurs.
- Carbohydrate metabolism: patients exhibit impaired glucose tolerance.
Target-organ damage and hypertension
The severity of clinical symptoms is largely determined by blood pressure levels. Patients often complain of persistent headaches, decreased visual acuity, cardiac pain (cardialgia), and shortness of breath.
Of particular clinical danger is malignant hypertensive syndrome. It is characterized by:
- Persistent, extremely high elevation of diastolic blood pressure.
- Severe retinopathy with optic disc edema, plasmatorrhagia, and hemorrhages in the fundus, which can lead to complete blindness.
- Development of hypertensive encephalopathy.
- Rapid progression of heart failure.
Polyuric stage and urinalysis
A decrease in relative urine density (isosthenuria) is observed from the very beginning of the development of the renal form of acute renal failure (ARF).
7–10 days after the onset of the oliguric period, the diuresis recovery stage (polyuric) usually occurs. In this phase, the volume of excreted urine increases, azotemia gradually decreases, and general clinical improvement ensues. However, massive diuresis carries a serious risk — the development of hypokalemia (potassium levels drop below 3.8 mmol/L). On an ECG, this condition manifests as ST segment depression, low voltage of the T wave, and the appearance of extrasystoles.
For the differential diagnosis of the causes of pathology, urine sediment microscopy is critically important:
| Urinary sediment elements | Possible cause of pathology |
|---|---|
| Scanty sediment | Prerenal or postrenal (prolonged obstruction) ARF |
| Numerous red blood cells | Urolithiasis, trauma, tumor, infection |
| Leukocyturia | Infectious process, immune or allergic inflammation |
| Eosinophils | Specific marker of an allergic reaction of the urinary tract |
Note: when assessing hematuria, it is important to remember a social problem — the possible simulation of renal colic by substance-dependent patients in order to obtain injections of narcotic analgesics.
Immunological features
A separate category is pauci-immune type of lesion. Its key feature is the almost complete absence of immune deposits in the renal glomeruli. The diagnostic marker of this condition is the presence of antibodies to neutrophil cytoplasm in the blood (ANCA). This type of lesion is strongly associated with systemic diseases, including microscopic polyangiitis and Wegener's granulomatosis.
Briefly: answers to topical questions
What are the characteristics of the stages of acute renal failure (oliguric, polyuric, recovery)?
The stages of acute renal failure are characterized by a sequential change in diuresis disorders and a change in blood metabolite levels.
- Oliguric stage (azotemic) — the peak period, during which diuresis is less than 400 ml of urine per day, residual nitrogen, urea, and bilirubin increase.
- Polyuric stage (diuresis recovery) — begins after 7–10 days, accompanied by the development of polyuria, a decrease in azotemia, general improvement, and a high risk of hypokalemia (less than 3.8 mmol/L).
- Stage of complete recovery (convalescence) — differs by the normalization of nitrogenous waste products and electrolytes; however, complete restoration of glomerular filtration does not occur in all patients.
What criteria are used to classify chronic kidney disease (CKD) by stages?
To classify chronic kidney disease by stages, it is mandatory to calculate the glomerular filtration rate (GFR) using the CKD-EPI formula. The serum creatinine concentration, patient's sex, age, and race are used as parameters for the calculation.
| CKD stage | GFR level (mL/min/1.73 m²) |
|---|---|
| G1 | >90 |
| G2 | 60-89 |
| G3a | 45-59 |
| G3b | 30-44 |
| G4 | 15-29 |
What clinical syndromes are distinguished in chronic renal failure?
As renal function declines and chronic renal failure progresses, the following syndromes develop:
- Asthenic syndrome — manifests as progressive general weakness, drowsiness, and rapid fatigue.
- Uremic encephalopathy syndrome — initially manifests as apathy, later accompanied by convulsive twitching and progressive depression of consciousness up to uremic coma.
- Dyspeptic syndrome — is a striking sign of the uremia stage, accompanied by nausea, vomiting, hiccups, anorexia (reaching aversion to food), and diarrhea.
To memorize metabolic disorders in kidney pathology, use the acronym "B.L.U.M.": Proteins (decrease in muscle mass), Lipids (atherosclerosis), Carbohydrates (impaired tolerance), Minerals (deficiency of iron, copper, zinc, calcium).
Class and exam questions
What are the risks of the diuresis recovery stage?
The main risk of the polyuric stage is the development of hypokalemia (potassium below 3.8 mmol/L) due to massive urine loss. On an ECG, this manifests as ST segment depression, a decrease in T wave voltage, and extrasystoles.
How to differentiate prerenal AKI using urinalysis?
In prerenal (as well as postrenal) renal failure, microscopy reveals an extremely scanty urinary sediment. At the same time, the renal form is accompanied by isosthenuria from the first days.
What is malignant hypertensive syndrome in renal failure?
This is a severe condition characterized by persistently high diastolic pressure. It leads to hypertensive encephalopathy, heart failure, and severe retinopathy capable of causing blindness.
What is the core mechanism of pauci-immune renal injury?
With this type, there are no immune deposits in the glomeruli, and ANCAs are detected in the blood. This is characteristic of pathologies such as Wegener's granulomatosis and microscopic polyangiitis.
What else to study on this topic
- Prerenal and postrenal causes of renal failure
- Mechanisms of drug-induced nephrotoxicity
- ANCA-associated vasculitis and Wegener's granulomatosis
- Pathogenesis of the polyuric stage of acute kidney injury
- Electrolyte disturbances and their ECG manifestations
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