Biochemical Exploration of the Kidneys PDF

BIOCHEMICAL EXPLORATION OF THE KIDNEYS  Paraclinical examination of the kidneys A. Urine examination B. Examination of some blood parameters C. Effort tests D. Samples of instrumental exploration of the parenchyma E. Radiological explorations F. Radioisotopic explor...

BIOCHEMICAL EXPLORATION OF THE KIDNEYS  Paraclinical examination of the kidneys A. Urine examination B. Examination of some blood parameters C. Effort tests D. Samples of instrumental exploration of the parenchyma E. Radiological explorations F. Radioisotopic explorations G. Puncture - renal biopsy  BC exploration of the kidneys The kidneys play a very important role in the body by: Urine formation; The excretion of waste resulting from the catabolism of endo or exogenous substances; Maintaining hydro-electrolytic and acid-base balance; Maintenance of colloid-osmotic pressure; Secretion/synthesis of substances such as: renin; erythropoietin; 1.25 diHO vitamin D3 ; PG Urine is formed as a result of: Glomerular filtration; Tubular reabsorption; Tubular secretion. As a result, the final normal urine: contains urea, creatinine, phosphates and does not contain glucose, proteins, bicarbonates. is characterized by certain physical characteristics: values of pH, density, volume, color, smell.  Blood examination non-protein N2 substances urea = 15 – 45 mg/dl creatinine = 0.6-1.2mg/dl uric acid = 2.5 – 7mg/dl other blood parameters blood sugar = 70-109 mg/dl total proteins = 6.4 – 8.4 mg/dl Na = 135 – 145 mEq/l K = 3.5 – 5 mEq /l Cl = 95 -109 mEq /l Ca = 9 – 11 mg/dl P = 3 – 4.5 mg/dl Mg = 2 – 3 mg/dl Bicarbonate – AR = 22-28 mEq/l  Urine examination pH in the morning  crystalluria​ qualitative quantitative per 24h volume normal oliguria anuria appearance: clarity, color, smell substances  = 1020-1025, proteins, carbohydrates, UBG, bile pigments Na+, K+, Cl - urea, creatinine, uric acid → Clearance Ca+, P, Mg+ oxalate, citrate, urate  BLOOD TEST Non-protein nitrogenous constituents Urea the main nitrogenous waste ← human metabolism it is synthesized in the liver the ureogenetic cycle allows the transformation of NH 3 , toxic, into a non-toxic compound (if it is maintained within normal value limits) is very soluble → general circulation → kidneys ↓ glomerular filtration tubular reabsorption ↓ urine (contains 40-70% filtered urea) a small part: → perspiration → intestine, where it is subjected to urease from the bacterial flora VN = 15-45 mg/dl varies depending on: dietary protein intake age: ↑ in newborns ↓ with age pregnancy - ↓ diuresis - ↑ in low water intake PV ↓ are rare in: terminal stages of liver failure some hereditary enzyme deficiencies (OCT) hemodilutions ↑ more frequent in: acute or chronic renal failure It is NOT a faithful parameter of glomerular function, being influenced by extrarenal causes situations of protein hypercatabolism - young people / various aggressions marked and chronic → uremic syndrome, with neurotoxic manifestations Creatinine comes from creatine synthesized predominantly by the liver (less by the kidneys) ↓ muscle and brain ATP ↓ creatine kinase phosphocreatine = energy reservoir ↓ muscle contraction creatinine = non-toxic product found in all biological fluids at the level of the kidney: glomerular filtrations; active tubular secretion (10-15%) VN = 0.6 – 1.3 mg/dl are not influenced by food (only 10% comes from food intake) depending - directly on the muscular mass of the subject decrease in children and malnourished increases in athletes - of pregnancy – decreases by increasing GF not significantly depending on age, because the decrease in excretion due to the decrease in GF is compensated by the decrease in production as a result of the decrease in muscle mass PV ↑ in renal failure, being a good indicator of the quality of glomerular filtration in extensive muscle injuries ↓ in muscle strength processes Apart from renal pathology, creatininuria can be considered as an indicator of proteinaceous muscle mass. Uric acid the final product resulting from purine catabolism: exogenous – degradation of food nuclear acids endogenous – catabolism of cellular nuclear acids - synthesized "de novo" it is found in all extracellular fluids in plasma, at pH = 7.4, the entire quantity of uric acid is in the form of monosodium urate it is mostly eliminated through the kidneys, through a complex mechanism: glomerular filtration retroresorption at the level of the proximal convoluted tube tubular secretion at the level of the Proximal Convoluted Tubule postsecretory reabsorption finally, the excreted fraction represents only 10% of the ultrafiltered fraction VN = 2.5 – 5 mg/dl in women 3 – 7 mg/dl in men Increased PV: Primary hyperuricemia​ increase in endogenous synthesis – idiopathic gout enzyme deficiencies deficiency of tubular secretion Secondary hyperuricemia​ excessive food intake increased catabolism of cellular nuclear acids malignant hemopathies cytolytic agents → require prevention by increasing diuresis and pH renal elimination defect renal failure (↑ urea, ↑ creatinine) metabolites that interfere with renal elimination mechanisms through competition (lactic acid, ketone bodies – hyperuricemia from DM; chronic alcoholism)  taking some medicines: diuretics; salicylates glycogenosis type I: glucodeose-6-phosphatase deficiency → ↑ production of ribose-6- phosphate, the precursor of an enzyme PRPP (phosphoribosylpyrophosphate), involved in the synthesis of IMP (inosinic acid), an intermediate in the synthesis of other purine nucleotides (AMP and GMP) ; In addition, the associated lactic acidosis interferes with tubular secretion. Decreased PV: Hypouricemia - much rarer hereditary xanthine oxidase deficiency – very rare hypoxanthine → xanthine → uric acid xo xo serious liver diseases – decrease in uric acid synthesis drugs that: favor the elimination / inhibit XO  EXAMINATION OF URINE Urine: final product of renal activity explains kidney function and disease it is easy to harvest, at different times, serially if necessary Physical properties Urine volume / 24 h = Diuresis ← balance between H2O loss and exogenous / endogenous intake (700 ml) VN = 2000 – 2500 ml = 1500 – 2000 ml minimum quantity = 500 ml 500 – 1500ml = facultative diuresis (urine); it depends on the balance H2O intake - losses Polyuria  2000 ml/day physiologic  ingestion of liquids by emotions cold extrarenal pathology​ DI = diabetes insipidus ADH is missing → urinary loss → 20 l/day urinary   H2O DM → osmotic diuresis 4-5-6l / 24h urinary  = 1035 – 1040 passenger: different infectious diseases: pneumonia, malaria, typhoid fever; cessation of asthma, paroxysmal tachycardia, pectoral angina, renal colic, epileptic seizures heart failure treated with: tonicard; diuretics edematous diseases: nephropathies (compensated Chronic Renal Failure); hepato - renal disease​ Chronic glomerulonephritis​ Chronic pyelonephritis Renal tuberculosis​ Nephroangiosclerosis Oliguria  1000 ml/day physiological : dry food regime profuse perspiration - effort  ( football player – weight loss by 5 kg ) - temperature  (ovens 3000 C) pathologic extrarenal - febrile conditions - pneumonia - hepatitis - uncontrollable vomiting​ - diarrhea → liquid losses - hemorrhagia - untreated heart failure - vascular decompensated liver cirrhosis - ascites / edema - pleurisy  kidney - acute glomerulonephritis (urinary quantity  , ρ  ) - nephrotic syndromes: ↑ serine elimination  ρ  - renal colic - decompensated renal sclerosis  Anuria = 0 (actually ± 50 – 100 ml / day) in renal colic  the reflex inhibits the contralateral kidney in renal nephropathies with  necrosis of the tubular epithelium = Acute Renal Failure  intoxication with sublimate trauma/tissue crushing (war, fires) septic abortions incompatible blood transfusion surgical trauma (postoperatory shock)  Appearance of urine N clear transparent sometimes - slightly fluffy, like a cloud = clouds  release mucus Disturbance - from emission / after  remove salts = renal sand but it clears is ← reheat is / 2-3 little CH3-COOH pyuria  cloudy Color of urine yellow - straw (more diluted) → orange → red (more concentrated) dark color  urochrome urobilin porphyrin color changes pale – watery – polyuria – DM/DI yellow – greenish (brown) – Icteric sclerae red - hematuria - cloudy - hemoglobin in urea - clear → oxide → black – porphyrinuria meat juice - chronic glomerulonephritis Red Pyramidon Algocalmin Antipyrin Sulfonamide Red beet Carrot black melanoma alkaptonuria green (blue) – treated with blue methylene The smell of urine slightly ammoniacal or bland urinary infections ← Proteus acetone (rotten apples) ← decompensated DZ pH = urine reaction with litmus paper/pH meter = 5.2 – 8.2 depends on alimentation meat ↓ pH (acidic) vegetable ↑ pH (alkaline) alkaline vomiting resorption edema urinary infections acid febrile illness renal tuberculosis​​ Chronic Renal Failure (std 0) DM with acid-ketosis drugs with acid radicals (ρ) Urinary density depends mainly on urea and NaCl (urodensimeter - calibrated at 15°C ) depends on the quantity / M of his constituents ρ = 1020 – 1025 – normosthenuria deviations - hypo stenuria = ↓ concentration capacity ↓ max urinary ρ around 1014 – 1020 - isosthenuria ρ = 1010 – 1014 (is ρ of plasma) = deproteinized plasma the most serious phase - subisostenuria ρ = 1006 – 1007 in chronic pyelonephritis Urine osmolarity determinated exclusively of electrolytes: Na + ; Cl – ; urea by cryoscopy in mOsm / l: 300 - 1400 Biochemical composition of urine Varies with: - age - sex - the geographical area may vary in the case of the same individual - alim (pH) - physical activity​ Organic elements 1) urea is metabolized in the liver  protein metabolism = 80% urinary N2 in urine / 24 h = 24 – 30 g "+" NaCl give the ρ of urine urea ↓ - nephropathies (Acute Renal Failure) - cirrhosis (the kidney is not affected) 2) uric acid  nucleoprotein catabolism; = 1.3 g / 24h (0.3 g – vegetarian diet) ↑ gout leukemia pneumonia urinary lithiasis burns ↑ ingestion of nucleoproteins 3) creatinine - nitrogenous substance = 1 – 1.5 g / 24h ↑ in persons with high muscle mass in the case of effort Inorganic elements 1) NaCl - as it is consumed, so much is eliminated = 10-15 g/day (salt-free diet - 5g/day) ↓ diet \ [salt] lose in excess perspiration diarrhea vomiting febrile diseases – pneumonia edematous states heart failure chronic hepatic / renal disease​​ ↑ > 20g High salt regime (over 35g/day is to be retained) Addison's disease = insufficiency adrenal cortex elimination of edema from - heart failure - chronic hepatic / renal disease​​ 2) Na+ - is found alone in 6-9 g/24h = 170-230 mEq/day ↓ Pyelonephritis congenital tubular dysplasia - polycystic kidney Acute Renal Failure / Chronic Renal Failure 3) K+ it is reabsorbed in the Proximal Convoluted Tubule it is excreted in the Distal Convoluted Tubule in exchange for H+ = 2.5 – 3.5 g/day = 70 – 90 mEq/day + Na+ = 5 very​ important in some diseases K 2 ↓ in hypo K + regime (meat > K+ ) diarrhea Acute Renal Failure nephrite with lose of K+ 4) Ca ++ ↑ Hyperparathyroidism​​ bones tumors multiple myeloma consumption ↑ of milk - patients with ulcer → calculosis ← treatment with CaCO3 – patients with ulcer 5) Mg + ↓ Acute Renal Failure Pathological substances in the urine PROTEINS normally does not exist with different doses = 40-80 mg/ day proteins with low molecular weight: 58000 – can pass through the renal filter and be reabsorbed proteinuria prerenal slightly crossed renal filter = paraproteins M < 60000 Waldenström's mglobulinemia malignant lymphogranulomatosis lymphosarcoma Bence-Jones proteinuria – thermostable - at 60° - ‡ by heating the urine to  60° it becomes clear  renal  damage to the renal filter or of the renal membrane acute glomerulonephritis Nephrotic syndrome Diabetic glomerulonephrosis Hypoxia of glomerular capillaries leukocytes​  pus ∙ in urological affections 1. acute / chronic pyelonephritis 2. renal tuberculosis 3. pyonephrosis 4. infected tumor 5. infected lithiasis 6. urinary retention - in prostatic patients Lipuria ∙ ← unsaturated fats acids, neutral fats, Cholesterol ∙ in Nephrotic syndromes / pyonephrosis /  bone fractures (bone marrow → blood → urine) ∙ deficiencies for recognition Cholesterol​  silhouette of some blocks other fats  Maltese cross Glycosuria ∙ Normal not exist ∙ presence in - general metabolic disease - DM - kidney disease that allows glucose resorption (normal blood sugar) ∙ glucose is osmotically active  polyuria   DM / Renal diabetes thirst ∙ transients 1. serious infectious diseases: typhoid fever meningitis encephalitis 2. acute/chronic intoxications: Pb; Ur; Hg 3. stroke: hemorrhages / thrombosis 4. hyperthyroidism 5. chronic liver diseases 6. acute phase of MI 7. pregnancy 8. acute pancreatitis Ketone bodies ∙ are acetic acid β-HO Butyric acid acetone ∙ in decompensated DM: precoma / coma ∙ very serious condition ∙ other situations in children – uncontrollable vomiting in adults - starvation bile pigments + bile acids Urobilinogen normal present Urobilin ↑ - hepatic disease ↓ - hepatic disease – mechanical jaundice Bilirubin - normal does not exist - there are liver diseases Bile acids - liver diseases Bile salts - Hey sample – S flower (drops in urine  bile salts)  MICROSCOPIC EXAMINATION After a centrifugation – 2000 rotations/min. – 5min → organized / unorganized sediment No sediment is formed in the cycle Sediment ⊃ epithelial cells 3 – 4 leukocytes / field 1 – 2 red blood cells / field other elements - cylinders urinals - single cylindric formation = casts of the distal tubules of the nephron 1. leukocytes A/C Pyelonephritis (  ) infection of the parenchyma 2. hyaline  proteins ‡ in tubes in Nephrotic Syndromes 3. granular  renal cell destruction 4. epithelial  epithelia of convoluted tubes 5. colloids – proteinaceous  lipids renal insufficiency 6. granulo-fatty – Nephrotic syndromes  cylindrical scraps and fats 7. pigmentation  hemoglobin, myoglobin, bilirubin Salts 1. urate crystals and uric acid 3. oxalate Ca 2. phosphates: Calcium; ammonia-Mg 4. CaCO3 Quantitative urinary sediment = Addis – Hamburger ∙ per min ∙ indications 3h at bed everything that urinates is measured, a sample is taken it is centrifuged at 3000 rotations for 5 minutes from the last cm3 it homogenizes → reading blade (smear) Red blood cells 1000/min leukocytes 2000/min = VN cylinders 5/min ∙ is used for​​  GN diagnosis > 200,000/min 5,000 – 10,000/min Pyelonephritis + 100,000 leuc/min + 1,000 red blood cells/min the evolution of GN today 2,000,000 Hematias tomorrow 1,000,000 - good prognosis then ↓ or ↑ - poor prognosis  BACTERIOLOGICAL EXAMINATION OF URINE Uroculture ∙ sterile test tube on the left ∙ with the right hand we remove the cork ∙ middle jet → test tube ∙ microbes are counted / mm3 -  100,000 – significant for urinary infection ∙ microbes  antibiotics  sensitivity to antibiotics Changes in the physical and chemical qualities of urine determine the so-called urinary syndrome, which occurs in different forms in renal or extrarenal diseases, along with other syndromes. I. Urinary syndrome from glomerular nephropathies ∙ glomerulonephritis ∙ glomerulonephrosis – Nephrotic syndrome II. Urinary syndrome for tubular nephropathies III. Urinary syndrome for interstitial nephropathies IV. Urinary syndrome for vascular nephropathies I. Urinary syndrome from glomerular nephropathies Acute diffuse GN Urine: 1. brown – dirty 2. oliguria → anuria (500-700ml) 3. ρ > : 1030 (tubular functions not affected) 4. protein = 5 g/l 5. red blood cells: Addis-Hamburger test 250,000 – 1,000,000 red blood cells /min ex amen microscopic: full field of red blood cells the appearance may persist even after healing 6. Infection + hematuria "+++" → gomerulonephritis in focus Infection, after 7 days = nephropathy by immune mechanism 7. Leukocytosis is not very important 8. Cylindruria ∙ 60% cases hyaline ∙ types hematic leukocytes granular  Chronic Pale urine Edematous form Nephrotic form Diuresis ↑ ↑ ρ ↓ → isosthenuria 1010 1020 Osmolarity ↓ ↓ ↓ Protein​​ 1-2 g/day 10-15 g/day Hematuria Discreet leukocyturia Cylinder "-" numerous Glomerulonephrosis Lesion = membranous glomerulitis due to: Systemic Lupus Erythematosus (SLE) Chronic nephritis Urine ∙ oliguria 500 – 700 ml ∙ ρ ↑  high proteinuria ∙ proteinuria = 50 - 60 g ‰ ∙ appearance: milky, slightly foamy ∙ lipuria = the presence of lipids in the urine → opalescent appearance ∙ hematuria ± in the forms of pure / impure glomerulonephrosis ∙ leukocyturia - ± ∙ cylindruria quantity, large: hyaline blood cells fat granulo-fatty  II. Urinary syndrome from tubular nephropathies ∙ Acute Renal Failure ∙ kidney shock ∙ acute tubular necrosis The oliguric - anuric stage The polyuric stage ∙ diuresis ↓ 50-200 ml ∙ diuresis 4000-6000 ml/24h ∙ dark brown color ∙ ρ ↓ (remain with isosthenuria → 6 months) ∙ ρ↓ 1002-1004 ∙ discrete proteinuria ∙ muscle proteinuria​ ∙ leukocyturia ∙ insignificant hematuria ∙ cylinder capacity ∙ insignificant leukocyturia ∙ hematuria ∙ insignificant cylinder ∙ removal: ∙ ↓↓ elimination of nitrogenous nitrogen catabolism products - ↑ progressive catabolism products in 3 months electrolytes III. Interstitial renal syndromes Affecting the distal tubes + the interstitium Acute pyelonephritis Urine 1. cloudy appearance due to urinary pus 2. ρ = normal value osm = normal value volume = normal value, but pollakiuria + dysuria 3. proteinuria – moderate 1 g ‰ 4. urinary tenesmus 5. minimal hematuria 6. leukocytosis – millions /min. 7. bacteriuria – significant urine culture: 100,000 bact/mm3 8. cylinders - leukocyte, granular Chronic pyelonephritis Urine 1. Pale appearance 2. V = ↑; polyuria – tries to compensate 3. ρ ↓ - isosthenuria 4. proteinuria ↓ 5. Non-essential hematuria 6. Bacteriuria! - significant:  100,000 bact/mm 3 - intermitent 7. Leukocyturia IV. Urinary syndrome from vascular nephropathies In: - renal artery stenosis - nephroangiosclerosis Urine ∙ pale ∙ proteins ↓ ∙ Red blood cells – few / field It assimilates kidney function → kidney separation: good – bad  Renal edematous syndrome ∙ is clinical ∙ initially palpebral edema - connective tissue is very lax. bigger in the morning → disappear in the evening facial edema → lunar appearance, O, Bouffi ∙ then edema → lower limbs, serous → anasarca ∙ have the same characters as cardiac ones. comprise the integuments entirely (1/2 upper) organs: larynx → hoarseness heart: cardiomegaly, deafening of heart sounds CNS - headache - memory disorder - cerebral edema ∙ characters soft fluffy white painless deep well ∙ pathogenic chains ↑ capillary permeability ↓ Oncotic pressure ↓ Glomerular Fraction ↑ tubular reabsorption - Na + - H2O Secondary hyperaldosteronism ↑ retroresorption - Na + - H2O  Acute diffuse GN – Ag – Ab conflict in all ↓ MB damage of the capillaries ↓ ↑ capillary - glomerular permeability - from the whole body → edema hematuria leukocyturia ↓ proteinuria plasma fluid with proteins → interstitium ↓ effective plasma volume ↓ glomerular filtration Plasma exudes into the interstitium ↓ activation of: the basal membrane; ↑ glomerular corpuscle; volume recovered from corpuscles ↓ plasma volume isotonicity Acute Renal Syndrome ↓ ↑ triggers the aldosterone mechanism ↓ retention of H2O retention of Na + in the renal tubule ↓ ↑ blood osmolarity ↓ ↑ ADH secretion Glomerulonephrosis – Nephrotic syndromes ↓ Oncotic pressure Lesion = membranous glomerulitis: breaking the basement membrane mesh → large amount of protein loss ↓ ↓ Oncotic pressure in capillaries ↓ Transuded fluid at the arterial head is not blindly reabsorbed at the venous head ↓ edema ↓ ↓ circulating plasma volume ↓ juxtaglomerular receptor volume excitability ↓ aldosterone ↓ Na + ↓ ↑ osm ↓ ↓ release of ADH ↓ H2O retention​ ↓ restoring the plasma volume but the oncotic pressure is ↓​ !!! Important : it intervenes at the point of departure Chronic nephropathies ↓ glomerular filtration (GF) normal reabsorption, but proteins that are missing in the blood 2) ↓ serines 3) ↓ globulins (↑α2) 4) ? ↑ lipemia = 3000 – 5000 mg% ↑ Cholesterol = 500 – 600 mg% ↑ Triglycerides 5) rapidly progressive atherosclerosis a) Myocardial infarction b) Stroke c) accentuation of renal sclerosis 6) ↓ Ca2+ 7) ↓ K+ 8) ↓ I+ 9) uremia 10) ↓ Plasma volume Renal failure syndrome  sudden / slow loss of renal capacity to maintain homeostasis  Toxic syndrome: ∙ retention of nitrogenous waste products ∙ acid-base, hydro-electrolyte balance disorders, ∙ disorders at the level of the whole organism Evolution → Acute Renal Failure / Chronic Renal Failure – the final state of all kidney diseases Acute Renal Failure ∙ prerenal diseases in which ↓ renal irrigation  ↓ GF (basal membranes are not damaged) a) functional - is revesible - they are: hemorrhagic fluid loss - vomiting - diarrhea - sweating b) organic  circulatory deficit is not corrected ∙ kidney organic renal disorders → tubular 1) serious ischemic alterations of duration: hemorrhages  lose fluids (vomiting, diarrhea, sweating, burns) traumatic shock crush syndrome operative shock Acute Renal Failure electrocution incorrect transfusions serious​ septic conditions  morphological lesions :​​ - break the membranes in fragments = tubulorhexis = necrosis in spots - renal interstitial edema 2) nephrotoxic  substances that concentrate and precipitate at the tubular level - sublimated (concentrated) - mushrooms - amanita phalloides - chloroform - sulfonamides (Biseptol) - CCl4 - Methemoglobin, hemoglobin - heavy metal salts: Au, Ag, Bi 3 ) hyperacute glomerular diseases :​ - pregnancy eclampsia - intoxication of a toxic-allergic nature: As, quinine - renal cortical necrosis  oligoanuria  suspension of renal filtration ↓ tubular retroresorption  water → interstitium ↓ edema ↓ tubal compression of intact tubes homeostasis disorders ∙ postrenal ureteral obstruction: stones extrinsic compressions cicatricial stenosis urethral/bladder ruptures < = pelvic fractures / prostate tumor - a pyelorenal (retrograde) infection also occurs Oligoanuric period → 6 – 14 days = ↓ diuresis ( 500 ml / 24h) clinical signs: digestive nervous hematological of uremia lung hyperhydration phenomena Acute Pulmonary Edema​ Cerebral edema Eclamptic/ tetanic seizures electrolyte disturbances irregular heart rhythm - ES; PT Kussmaul / Cheyne – Stockes respiration neuro-muscular asthenia humoral signs ↓ osmosis  electrolytes: Na+ ↓; Cl- ↓; K+ ↑ ! ↓ Alkaline reserves = ↓ pH  progressive metabolic acidosis diagnostic – on ↑ nitrogen retention product : - urea 50 - 60 mg% - creatinine 5 - 10X - uric acid evolution - very serious, many die artificial kidney - correction of this disorder Polyuric period: ∙ the tubules begin to regenerate ⊃ the simple epithelial cells ∙ diuresis ↑ slowly from one day to the next → 6-9 l / day ∙ isotenuric urine ∙ !!! the danger of eliminating electrolytes: Na+ and K+ → exicose (H2O elim) alkalosis hypo K+ ∙ full recovery in months → years ∙ some remain with a functional deficit Chronic Renal Failure ∙ intact nephron theory ∙ causes – order of appearance Chronic pyelonephritis Glomerulonephritis​ nephroangiosclerosis diabetic capillary glomerulosclerosis: Syndrome KW amyloid glomerulo-nephrosis polycystic kidney ∙ occurs at → 50% functional nephrons (2 million) – responds only to basic requirements ∙ compensatory mechanism:​ Hypertrophy of intact nephrons ↑ blood pressure polyuria, nocturia, ↑ osmotic / nephron charge due to destruction, further  homeostasis disorders → humoral disorders, then clinical = chronic uremia Stages Compensated Chronic Renal Failure Decompensated Chronic Renal Failure – homeostatic disturbances „-” clinical signs uremia - "+" clinical manifestations uremic coma Compensated Chronic Renal Failure nephrons = 50% - 25% stage polyuria without nitrogen retention - nocturia - hypostenuria - ↓ Cl, ↓ glomerular function, ↓ renal plasma flow fixed nitrogen retention - urea = 60 - 70mg% - it's not harmful - creates osmotic diuresis - polyuria - isosthenuria Decompensated Chronic Renal Failure functional nephrons​  25% pseudonormaluria → isosthenuria then oliguria humoral picture 1. urea  70 mg% 2. uric acid 3. creatinine 2 - 5 - 10 times 4. xanthoproteins reaction 5. electrolyte disturbances (Na+; K+) 6. Hyperhydration or cellular dehydration 7. metabolic amyloidosis – finally Uremia – nephrons  10% altered general condition: headache, fatigue, hypothermia, arterial hypotension, fever, tachycardia symptoms nervous Cardio-vascular respirators​ in nephropathies summer pier skin: pale yellowish dirty Digestive system vomiting - ammoniacal hematemesis - melena bloating → abdominal pain diarrhea fried tongue ulcerative stomatitis mucosal hemorrhages The neuro-psychic system daytime sleepiness – insomnia at night Osteotendinous hyperreflectivity patella clonus Babinski sign delirium / manic agitation → coma Respiratory system Acute pneumopathies respiration - K; Ch-S pleurisy – right lung base (Nephrotic syndrome) The cardio-vascular system Hemorrhagic syndromes  thrombocytopenia vascular fragility dry uremic pericarditis severe myocarditis Humoral syndrome urea creatinine uric acid ↑ N2 remaining non-protein Acidic pH acid - base and hydro - electrolytic imbalances = the most serious causes of this disorder Uremic coma delirium differential diagnosis with diabetic coma, hypoglycemia, cerebral hemorrhage, hepatitis they usually die / complications Acute Pulmonary Edema high blood pressure septicemias