Stages and tasks of the diagnostic process
The clinical diagnosis in nephrology is based on sequential data collection and the synthesis of leading syndromes. This allows for precise nosological diagnosis: identifying a specific disease (e.g., isolated acute or chronic glomerulonephritis, amyloidosis) or establishing kidney involvement in systemic pathologies (systemic lupus erythematosus, polyarteritis nodosa, hemorrhagic vasculitis).
Comprehensive analysis of anamnesis and laboratory data is necessary to determine the etiology of the process—whether infectious, allergic, drug-induced, or associated with metabolic disorders (purine, carbohydrate).
Ultimately, diagnosis addresses three tactical tasks:
- Assessment of the disease prognosis.
- Identification of indications for active therapy (glucocorticoids, cytostatics, monoclonal antibodies).
- Consideration of the risks of complications that treatment itself may provoke.
Assessment of pathological process activity
To determine the degree of activity of an autoimmune or inflammatory process, a wide range of clinical and laboratory markers is used.
- Clinical presentation: increased proteinuria and hematuria, worsening arterial hypertension, appearance of edema, or the development of full-blown nephrotic and nephritic syndromes.
- General inflammatory changes: elevated ESR, dysproteinemia (mainly due to an increase in $\alpha_2$-globulins), elevated C-reactive protein levels.
- Immunological activity: detection of antinuclear factor (ANF) and LE cells, hypocomplementemia (decreased levels of complement components), high concentrations of circulating immune complexes (CIC).
To refine the diagnosis, it is essential to evaluate specific autoantibodies (anti-glomerular basement membrane, ANCA, rheumatoid factor) and serum proteins, particularly type II cryoglobulins.
Assessment of functional renal state
To determine the stage of the pathological process, basic functional parameters are analyzed. These include urine relative density (reflecting concentration function), serum creatinine levels, and its clearance, which indicates the glomerular filtration rate.
The development of long-term chronic renal failure (CRF) is indicated by systemic disorders:
- Electrolyte imbalance, primarily hyperkalemia.
- Acid-base balance disorders.
- Progressive anemia caused by a drop in erythropoietin synthesis.
- Morphometric changes: decreased kidney size detected on ultrasound or plain radiography.
Mechanisms of progression and the concept of nephroprotection
Most chronic diffuse kidney diseases share a common pattern: they steadily progress regardless of the initial cause. The ultimate outcome is the loss of nephrons, CRF, end-stage renal disease, and the need for hemodialysis or transplantation.
Today, a paradigm shift has occurred: alongside immune inflammation, a key role is played by non-immune mechanisms—hemodynamic disorders. These are driven by the excessive production of angiotensin II, which causes spasm of the efferent glomerular arteriole. Additionally, systemic arterial hypertension is transmitted to the capillaries. Intrarenal hypertension and hyperfiltration ensue. High intracapillary pressure damages the filter, sharply increasing proteinuria, which itself acts as a major driver of disease progression. This stimulates the production of mesangial matrix and leads to glomerulosclerosis.
RAAS blockade as the basis of protection Immunosuppression alone is insufficient for treatment because fibrosis progresses in parallel. Blockade of the renin-angiotensin-aldosterone system (RAAS) is recognized as the baseline strategy for nephroprotection. ACE inhibitors lower intraglomerular pressure and have a pronounced antiproteinuric effect. According to the REIN study, the use of ramipril reliably slows the progression of CRF, making this drug class the only one with convincingly proven efficacy in chronic kidney disease.
Briefly: answers to topical questions
What formulas are used to calculate the glomerular filtration rate (GFR) based on serum creatinine?
To calculate the glomerular filtration rate (GFR) based on serum creatinine, the Cockcroft-Gault formula and the CKD-EPI formula are used.
- Cockcroft-Gault formula — uses individual patient parameters (age, body weight, serum creatinine), with the result multiplied by 0.85 for women.
- CKD-EPI formula (CKD-EPI equation) — proposed by the Chronic Kidney Disease Epidemiology Collaboration. It is calculated as: GFR = 141 × min(Serum Cr / k, 1)^a × max(Serum Cr / k, 1)^(-1.209) × 0.993^(age) × 1.018 [if female] × 1.159 [if Black].
The Reberg-Tareev test is also used as a clinical standard for assessing endogenous creatinine clearance.
Which specific cytostatics are used for active therapy of chronic glomerulonephritis?
In the cited sources, specific cytostatics for the treatment of glomerulonephritis are indicated as follows:
- Cyclophosphamide — used as a cytostatic in baseline immunosuppression for idiopathic membranoproliferative glomerulonephritis along with prednisolone; also indicated as the drug of choice for high clinical and laboratory activity of glomerulonephritis in IgA vasculitis in combination with glucocorticoids.
- Mycophenolate mofetil — used as a cytostatic option for baseline immunosuppression in idiopathic membranoproliferative glomerulonephritis along with prednisolone.
For nephritic syndrome with rapid deterioration of renal function in idiopathic membranoproliferative glomerulonephritis, sources indicate an aggressive start with plasmapheresis and methylprednisolone pulse therapy, followed by a transition to a baseline cytostatic regimen.
To remember the hemodynamic cascade of glomerular destruction, use the "S-P-P-S" mnemonic: Spasm (of the efferent arteriole) → Pressure (intraglomerular hypertension) → Proteinuria → Sclerosis.
Class and exam questions
Why are ACE inhibitors prescribed even when blood pressure is normal?
In nephrology, ACE inhibitors are used not only as antihypertensive agents but also as the basis of nephroprotection. They relieve efferent arteriolar spasm, lower intraglomerular pressure, and reduce proteinuria, preventing nephron loss.
Which parameters indicate the development of chronic renal failure (CRF)?
The onset of CRF is indicated by decreased creatinine clearance, the appearance of hyperkalemia, anemia (due to erythropoietin deficiency), acid-base disturbances, and a physical reduction in kidney size.
What is the non-immune mechanism of kidney disease progression?
The non-immune mechanism is associated with hemodynamic imbalance. Excess angiotensin II causes intrarenal hypertension and glomerular hyperfiltration, which injures the renal filter, induces proteinuria, and triggers glomerulosclerosis.
What else to study on this topic
- Clinical manifestations and pathogenesis of nephrotic and nephritic syndromes.
- The impact of systemic lupus erythematosus and polyarteritis nodosa on renal tissue.
- Limitations and risks of active immunosuppressive therapy with glucocorticoids and cytostatics.
- The role of carbohydrate and purine metabolism disorders in the progression of renal pathology.
- Differential diagnosis based on autoantibody marker analysis (ANCA, LE cells, ANF).
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