Biochemical markers and electrolyte imbalance
Blood tests make it possible to accurately assess the degree of kidney damage and risks to homeostasis. With pronounced metabolic shifts, the following changes are observed:
- Protein metabolism: hypoproteinemia is of critical importance. If the albumin level drops below 1 g/L, plasma oncotic pressure sharply decreases. This leads to a reduction in circulating blood volume, provoking arterial hypotension and hypovolemic shock.
- Lipid metabolism: massive protein loss is always accompanied by hyperlipidemia (an increase in cholesterol and triglycerides), which serves as reliable confirmation of nephrotic syndrome.
- Electrolytes and acid-base balance (ABB): hyponatremia (less than 135 mmol/L), hyperphosphatemia, and hypocalcemia are typical. With decreased cardiac output, metabolic acidosis develops rapidly (pH < 7.35). The main threat is hyperkalemia — it manifests on the ECG as a tall, peaked T wave and carries the risk of sudden cardiac arrest.
Criteria for nephrotic syndrome (NS)
Classic nephrotic syndrome manifests with severe disorders of water-salt, lipid, and protein metabolism. Its diagnosis relies on a strict triad:
- Massive proteinuria: urinary protein loss exceeds 3.0–3.5 g per day.
- Edema syndrome: fluid actively accumulates in tissues, causing massive edema up to anasarca, and also transudates into serous cavities (hydrops).
- Laboratory shifts: dysproteinemia and hyperlipidemia.
Interestingly, the "pure" variant of this syndrome is not characterized by elevated blood pressure and the presence of red blood cells in the urine. However, patients are at high risk of thrombotic complications (especially pulmonary embolism and renal vein thrombosis). This is due to hypercoagulation caused by elevated levels of fibrinogen and clotting factors V, VII, VIII, and X.
Oliguric (azotemic) stage
This critical condition begins with a sharp drop in diuresis (up to anuria) as early as the first day. The body rapidly accumulates nitrogenous wastes (creatinine), and hyperhydration occurs.
An acute uremia syndrome develops, affecting all systems:
- General manifestations: pronounced adynamia, nausea, and vomiting.
- Neurology: pathological drowsiness and muscle twitching.
- Digestive tract: abdominal pain, liver enlargement (hepatomegaly).
- Respiratory system: due to mounting acidosis and early pulmonary edema, severe shortness of breath appears.
Etiology and pathways of damage
Renal (parenchymal) pathologies are the largest group of causes. According to the extent of tissue involvement, they are divided into:
- Bilateral: glomerulonephritis (the most frequent cause), diabetic nephropathy, polycystic kidney disease, and tubulointerstitial nephritis.
- Unilateral: injuries, tumors, tuberculosis, pyelonephritis, or solitary cysts.
Mechanisms of development also differ. Thus, the immune complex type is characteristic of lupus nephritis, hemorrhagic vasculitis, and post-streptococcal glomerulonephritis. In this type, complexes are deposited in the tissues, giving a granular fluorescence pattern upon immunofluorescence. In contrast, the hematogenous route involves the seeding of staphylococci from external foci (felon, mastitis). In this case, purulent infiltration begins in the cortex and spreads to the interstitial tissue.
Briefly: answers to topical questions
What ECG changes, besides a tall peaked T wave, are observed in severe hyperkalemia?
In addition to tall, peaked T waves, progressive conduction disturbances are registered on the ECG as hyperkalemia worsens.
- Prolongation of the PR interval — occurs as potassium levels rise.
- Widening of the QRS complex — accompanied by the fusion of the complex with the T wave, giving it a sinusoidal appearance.
- Disappearance of the P wave — or its significant broadening.
- Shortening of the QT interval — noted in the early stages of increasing potassium.
- Atrioventricular block — develops when potassium levels exceed 9 mmol/L.
- Ventricular arrhythmias — ventricular tachycardia or ventricular fibrillation, carrying the risk of sudden death.
How does nephritic syndrome clinically differ from nephrotic syndrome?
Clinically, nephritic and nephrotic syndromes differ in the characteristics of edema, severity of protein loss, as well as the presence of hematuria and hypertension.
| Sign | Nephrotic syndrome | Nephritic syndrome |
|---|---|---|
| Edema | Pronounced, up to anasarca | Typical localization — face (pale puffiness) |
| Proteinuria | Massive, greater than 3.0–3.5 g/day | From moderate to significant |
| Hematuria | Not characteristic | Of renal origin, "meat slops" colored urine |
| Arterial hypertension | Not characteristic | Progressive, with an increase in diastolic pressure |
By what laboratory criteria is glomerular hematuria distinguished from nonglomerular hematuria?
A glomerular source of bleeding is confirmed by the detection of specific elements in the urinary sediment upon microscopy.
- Dysmorphic red blood cells — misshapen forms of red blood cells, which are detected predominantly using phase-contrast microscopy.
- Red blood cell casts — their presence in the sediment reliably confirms the glomerular origin of hematuria.
The persistent nature of hematuria with the presence of dysmorphic red blood cells requires the mandatory exclusion of glomerulonephritis.
What types of casts are found in the urinary sediment in glomerulonephritis?
In glomerulonephritis, the following casts are described in the urinary sediment according to the cited sources.
- Red blood cell casts — found in acute glomerulonephritis; in nephritic syndrome, they are detected predominantly and confirm the glomerular source of bleeding.
- Cellular casts in lupus nephritis — can be erythrocytic, granular, hemoglobin, or mixed.
- Granular and mixed casts — indicated among possible urinary sediment changes in renal involvement in SLE / lupus nephritis.
The "LOTS-LITTLE" rule for pure nephrotic syndrome: LOTS of protein in the urine (proteinuria), LOTS of lipids in the blood and fluid in the tissues (edema), but LITTLE protein in the blood (hypoalbuminemia) and NO hypertension with hematuria.
Class and exam questions
Does blood in the urine always indicate serious kidney pathology?
Not always. There is march (sports) hematuria, which occurs after heavy physical exertion. However, the persistent nature of the bleeding or the detection of altered (dysmorphic) erythrocytes requires the exclusion of glomerulonephritis.
Why does nephrotic syndrome carry a risk of thrombosis?
The pathology is accompanied by hypercoagulation. There is an increase in the concentration of fibrinogen, clotting factors (V, VII, VIII, X), and fibrinolysis inhibitors, which frequently leads to renal vein thrombosis or pulmonary embolism.
What is the danger of a sharp drop in blood albumin?
Albumin retains fluid within the vascular bed. When it drops below 1 g/L, oncotic pressure catastrophically decreases, circulating blood volume diminishes, which can provoke hypovolemic shock.
What else to study on this topic
- Features of the differential diagnosis of hematuria (march hemoglobinuria vs. glomerulonephritis).
- Mechanisms of hypercalcemia development in acute skeletal muscle necrosis.
- The role of systemic connective tissue diseases (SLE, vasculitis) in the development of nephropathies.
- Pathogenesis of purulent infiltration of the interstitial tissue in apostematous nephritis.
- Features of renal pathology screening during pregnancy management and arterial hypertension.
Master the entire topic in the "Propaedeutics" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on «Diagnosis of Nephrological Pathologies» and 3,152 more pages on the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 113 video lessons on the subject
Other topics in the "Urinary System" section
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.