Nephrology for Students KFU General 2023 PDF

Nephrology (from Greek nephros "kidney", combined with the suffix -logy, "the study of") is a specialty of medicine and pediatrics that concerns itself with the kidneys: the study of normal kidney function and kidney disease, the preservation of kidney health, and the treatment of kidney disease, fr...

Nephrology (from Greek nephros "kidney", combined with the suffix -logy, "the study of") is a specialty of medicine and pediatrics that concerns itself with the kidneys: the study of normal kidney function and kidney disease, the preservation of kidney health, and the treatment of kidney disease, from diet and medication to renal replacement therapy (dialysis and kidney transplantation). The main kidney functions are: - remove waste products from the body - balance the body's fluids - maintenance of electrolyte balance - maintenance of acid-bace balance - produce an active form of vitamin D that promotes strong, healthy bones - control the production of red blood cells - release hormones that regulate blood pressure Clinical urine analysis color relative density of urine odor turbidity acidity, or pH. albuminuria glucosuria urinary sediment Creatinine is a breakdown product of creatine phosphate in muscle, and is usually produced at a fairly constant rate by the body (depending on muscle mass). Creatinine is removed from the blood chiefly by the kidneys, primarily by glomerular filtration, but also by proximal tubular secretion. Little or no tubular reabsorption of creatinine occurs. Creatinine in the serum is mesured in mg/dl Metric units – mg/dl Conversion factor – is 88.4 SI units -µmol/l International system units mg/dl x 88.4 = µmol/l Serum creatinine increases in such situations as: - acute and chronic renal failure; - acromegaly and giantism; - taking nephrotoxic drugs (mercury compounds, sulfonamides, thiazides, antibiotics from the group of aminoglycosides, cephalosporins and tetracycline, barbiturates, salicylates, androgens, cimetidine, trimethoprim-sulfomethoxazole); - mechanical, operating, massive muscle damage; - crush syndrome - radiation sickness. - false increase: it is possible with increased concentration in the blood of some endogenous metabolites (glucose, fructose, ketone bodies, urea, some drugs - ascorbic acid, levodopa, cefazolin, cefaclor, reserpine, nitrofurazone, ibuprofen); - prevalence of meat in the diet; - hyperthyroidism; - hypohydration Creatinine decreases in such situations as: - starvation, decreased muscle mass; - reception of corticosteroids; - pregnancy (especially 1 and 2 trimester); - vegetarian diet; - hyperhydration; - myodystrophy. Glomerular Filtration Rate (GFR) is the volume of fluid filtered from the renal (kidney) glomerular capillaries into the Bowman's capsule per unit time. Normal GFR varies according to age, sex, and body size, and declines with age. Therefore, the measured value of GFR is accepted to be related to the value of the "standard" body surface of 1.73 m2. For young people, normal GFR is 120-130 ml / min / 1.73 m2 (standard deviation 20- 25 ml / min / 1.73 m2). In children the level of adults is reached by 2 years. GFR can be measured using clearance methods, with radioactive tracers. Also a number of formulas have been devised to estimate GFR (or Ccr values)on the basis of serum creatinine levels. The clearance of exogenous substances (which are injected into the blood): such as inulin, 51Cr-EDTA (ethylenediaminetetraacetic acid), 99mTcDTPA (diethylenetriaminepentaacetic acid), 125I-iothalamate and iohexol — are the most accurate clearance methods for evaluating the kidney function. They remain the "gold standard" for measuring GFR! Measurement with radioactive tracers GFR can be accurately measured using radioactive substances, in particular Chromium-51 and Technetium-99m. These come close to the ideal properties of Inulin (undergoing only glomerular filtration) but can be measured more practically with only a few urine or blood samples. Radioisotope methods of GFR research allow us to separately assess the functional state of the right and left kidneys, which is important in diseases with unilateral lesion, some kidney anomalies, etc. The evaluation of GFR for the clearance of an endogenous substance - creatinine, which enters the blood naturally in the process of self-renewal of muscle tissue at approximately constant rate, is more convenient, but less accurate, than the clearance of exogenous substances The formula for evaluating GFR for creatinine clearance you can see Scr = Ucr x V / PCr V - the volume of urine collected per day, ml; UCr - concentration of creatinine in daily urine; SCr - the serum creatinine concentration at the end of the sample. Pcr - and the plasma concentration (Pcr). GFR should be corrected for their actual body surface area (BSA) There are Alternative methods - calculation of GFR for easily measurable parameters. Since the beginning of the 1970s, attempts have been made to develop a formula that would allow, by determining the level of serum creatinine and several additional parameters that affect its formation in the body, to obtain a calculated GFR, closest in value to true GFR, measured by the inulin clearance or other precise methodsADULT GFR ESTIMATING EQUATIONS : Cockcroft- Gault formula GFR = (140-age) x Bm(kg) x K/Scr (µmol/l) K male = 1 K female = 2 MDRD(Modification of Diet in Renal Disease) CKD- EPI (Chronic Kidney Disease Epidemiology Collaboration) Serum Cystatine C -is a more accurate marker of GFR than creatinine for: - for patients with stages 2-5 of CKD - for the elderly patients (> 65 years) - patients with type 2 diabetes with CKD - patients after kidney transplantation - for patients after spinal trauma - patients with cirrhosis of the liver - children CKD- EPI creatinine- cystatin C GFR= 177.6Ч (Cr (mg/dl)) - 0.65 х (serum Cys C (mg/l)) -0.57 х age Сhronic renal failure - the outcome of chronic kidney disease (CKD) Metabolic diseases (diabetes, gouty nephropathy, kidney amyloidosis …) vascular diseases (hypertension, ischemic kidney disease...) Glomerulonephritis Tubulointerstitial nephropathies (primary, secondary with obstructive, cystic and other kidney diseases) Renal neoplasms Impaired development of the urinary system Injuries of urinary track system Arenial conditions Definition- CKD is defined as abnormalities of kidney structure or function, present for > 3 months, with implications for health GRADATIONS OF ALBUMINURIA ALB (mg) / CR (g) "Optimal" - 2000 mg / g). Criteria for CKD (either of the following present for >3 months) : Markers of kidney damage (one or more): Albuminuria (AER≥30 mg/24 hours; ACR≥30 mg/g [≥3 mg/mmol]) Urine sediment abnormalities Electrolyte and other abnormalities due to tubular disorders Abnormalities detected by histology Structural abnormalities detected by imaging History of kidney transplantation Decreased GFR: GFR< 60 ml/min/1.73 m2 (GFR categories G3a-G5 Anemia of renal genesis Reduced synthesis of erythropoietin (interstitial fibrosis) Hyperparathyroidism (fibrosis and bone marrow calcification, inhibition of the effect of Epo on blast cells, stimulation of erythrocyte apoptosis) Blood loss (blood sampling, bleeding and hemorrhage) Hemolysis (hyperparathyroidism, acidosis) Inflammatory diseases Deficiency of plastic materials - iron, protein, vitamins Hyperparathyroidism is an increased parathyroid hormone (PTH) levels in the blood. - Secondary hyperparathyroidism (SHPT) refers to the excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels) and associated hyperplasia of the glands. Hyperkalemia - unexpected nausea, vomiting ; - intestinal atony pain in the stomach of varying intensity; - increased weakness and fatigue of the body; - Muscle hypotension, muscle paralysis, pain in the muscles ; - fainting (can occur quite often); - decreased sensitivity and uncomfortable sensation tingling in the lower limbs and lips; - detachment and apathy of a person; - bradycardia, arrhythmia, ECG changes Principles of treatment of CKD beginning as early as possible diet and lifestyle correction are of great importance the importance of regular surveys to check the efficacy and safety of therapy many components of nephroprotective therapy have an increased risk of complications with reduced renal function continuity of treatment importance of active participation of the patient, self- control.Schools of patients with CKD Indications for renal replacement therapy in CKD - symptoms of uremia (serosite, acid-base (acidosis) and electrolyte balance, skin itching - impossibility to control the status of hydration and / or blood pressure conservatively - progressive decline in dietary status, refractory to dietary interference - encephalopathy and cognitive impairment revealed with a decrease in residual renal function Glomerular Diseases a large group of diseases of different pathogenesis, occurring with the damage of renal glomeruli Сlinical symptoms of glomerular lesions : isolated microhematuria - recurrent gross hematuria - isolated proteinuria - isolated urinary syndrome (microhematuria with moderate proteinuria) - nephritic syndrome (acute or chronic) - nephrotic syndrome +/- arterial hypertention - syndrome of rapidly progressive nephritis (proteinuria, hematuria, fast-growing renal dysfunction) - urinary syndrome in combination with arterial hypertension and slowly progressive renal dysfunction NEPHROTIC SYNDROME proteinuria more than 3.5 g / day - edema - hypoproteinemia, hypoalbuminemia +/- hyperlipidemia Structural damage of glomerular filtration barrier → massive renal loss of protein (hyperproteinuria) → reactively increased hepatic protein synthesis If protein loss exceeds hepatic synthesis (usually with a loss of protein > 3.5 g/24 hours) → hypoproteinemia/hypoalbuminemia, initially with both normal GFR ↓ Serum albumin; → ↓ colloid osmotic pressure→ edema(especially if albumin levels are < 2.5 g/dL) Loss of antithrombin III, protein Cand protein S, increased synthesis of fibrinogen, and loss of fluid into the extravascular space → hypercoagulability Sodium retention → possible hypertension NEPHRITIC SYNDROME: proteinuria less than 3.5 g / day - edema - arterial hypertension - microhematuria Inflammation → cytokine release → glomerular capillary damage Porous glomerular basement membrane → leakage of proteins and RBCs → nephritic sediment (all blood components are detectable on urinalysis) Proteinuria (< 3.5 g/24h): leakage of proteins Hematuria: leakage of RBCs, which stick together and form red blood cell casts in the renal tubules Oliguria: inflammatory infiltrates reduce fluid movement across the membrane (↓ GFR) Azotemia: inflammation prevents sufficient filtering and excretion of urea Salt retention → intravascular volume expansion → hypertension and edema Ethiology: - hereditary / genetic - idiopathic - within the framework of systemic diseases - secondary (medicinal, associated with infections, paraneoplastic Damage mechanisms: - cytokines - immune complexes - oxidative molecules - antibodies - paraproteins - complement - defects of collagen Damage Localization: mesangium -endothelium of glomerular capillaries -podocytes -glomerular basement membrane - capsule of glomerulus (Bowman's capsule) Morphological Damage Profiles in Glomerulonephritis minimal-change disease focal segmental glomerular sclerosis membranous nephropathy mesangiocapillary glomerulonephritis membranoproliferative glomerulonephritis focal proliferative glomerulonephritis diffuse proliferative glomerulonephritis extracapillary glomerulonephritis focal necrotising glomerulonephritis focal global and segmental glomerulosclerosis ( as an outcome of any nephropathy) diffuse nephrosclerosis Besides glomerulonephritis the category of glomerular damages include: - diabetic nephropathy - amyloidosis and other paraproteinemic damage to the glomerular apparatus - some genetically determined diseases (collagen pathology, diseases of accumulation etc.) - thrombotic microangiopathy Сlinical Recognition: - history data -assessment of the above symptoms characterizing the type of kidney damage - evaluation of extrarenal manifestations (if any) Essential components for differential diagnosis: - additional laboratory tests - morphological data obtained in the study of renal biopsy Kidney biopsy nephrotic syndrome - proteinuria more than 1 gram - persistent or glomerular hematuria - renal parenchymal hypertension unclear origin - renal AKI of unknown etiology with systemic symptoms, anuria over 3 weeks Contraindications to biopsy : the presence of a single functioning kidney (congenital or acquired pathology); - anatomical anomalies of the urinary system; - hydronephrosis (on one or two sides); - symmetrically reduced in size kidneys (