Kidneys pathology. (Subject 17) презентация

volume and composition of body fluid by filtration of the blood and selective reabsorption or secretion of filtered solutes.

The kidneys take their blood supply directly from the aorta via the renal arteries; blood is returned to the inferior vena cava via the renal veins

The kidneys are critical in regulating the internal environment of the body.

regulation:
Renin / Angiotensin / Aldosteron;
Sodium balance;
Pressure natriuresis

Clearance:
Products of metabolism;
Drugs and toxins;

ml per day.

Polyuria - increase the daily amount
of urine are usually caused by:
- absorption of edema, transudate, exudate;
- states after feverish;
- primary aldosteronism;
- hyperparathyroidism;
- nephrosclerosis;
- diabetes and diabetes insipidus

Oliguria - a reduction of daily amount
of urine are usually caused by:
- febrility;
- heart disease;
- acute renal failure;
- nephrosclerosis.

Anuria - a lack of urine,
less than 50 ml per day.
- acute renal failure;
- severe nephritis;
- meningitis (reflex);
- poisoning;
- tetany;
blockage of the urinary tract
tumor or stone

polyuria as a result of increased drinking, diuretics food.
Pathological hypohromuriya is developed due to:
- diabetes;
- diabetes insipidus;
- nephrosclerosis.

Color of urine

Normally, urine is amber or straw-yellow color.
Changes in urine color is possible with a number of
physiological and pathological conditions.

Hyperhromuria is physiological if it’s caused by oliguria as a result of limit drinking, sweating, eating carrots in the food.
Pathological hyperhromuria
is developed due to:
- diarrhea;
- toxicoses;
- fever;
- vomiting;
- liver disease, heart disease;
- hemolytic state.

a vessel in it it's easy to turbidity.
Turbidity of urine caused by crystals, cellular elements, bacteria, mucus, and fat.

The reaction of the urine is normal when pH is 5,5-7,0.

Acidic:
- diabetes (predkoma, coma);
- fevers;
- starvation;
- renal failure;
- tuberculosis of kidneys;
- leukemia;
- hypokalemic state (paradoxical aciduria)

Alkaline:
- haematuria;
- after vomiting and diarrhea;
-resorption of exudates, transudate;
- taking soda and mineral water;
- hyperhloremic acidosis;
- renal tubular acidosis;
- chronic urinary tract infections

Pathology of urine рН:

to 1.025 in the adult.

Hypostenuria - is low relative density of urine. It indicates that concentrating function of the kidneys has lost:

-in the morning portion of healthy individuals;
-in febrile patients;
-a reduced amount of urine;
-with amyloid and lipoid nephrosis;
-diabetes mellitus, glycosuria;
-hyperparathyroidism, etc.

-diabetes insipidus;
-resorption of edema and inflammatory infiltrates;
-chronic pyelonephritis;
-chronic nephritis;
-chronic renal failure;
-nephrosclerosis;
- glomerulonephritis.

Isostenuria - an absence of specific gravity‘s daily deviations. It
means that the diluting and concentrating functions of the
kidneys have both been lost:
-the latest stage of hronic renal failure;
-severe subacute and chronic nephritis.

Hyperstenuria - is the high
relative density of urine to ,030-
1,034 and often can be caused by
extra renal disturbances:

urinary protein excretion exceeding
150 mg/day.
The mechanism of proteinuria may be related to 2 aspects:
Molecular barrier injury: holes on glomerular basement membrane (GBM) become larger, plasma protein can pass through the GBM into the urine;

Charge barrier injury: loss of negative charge (glycoprotein) within GBM, plasma protein (with negative charge) can pass through the GBM into urine.

of a disease. The level of proteinuria is generally less than 1 g/day and is never associated with edema.
Postural (orthostatic)
Febrile
Exercise-induced
Pathological proteinuria results from glomerular or tubular disorders. It is characterized by persistent and severe intensity - more than 3.5 g/l.
Tubular:
Inherited - Cystinosis, Wilson disease, Lowe syndrome);
Acquired - Antibiotic-induced, Interstitial nephritis, Acute tubular necrosis, Heavy metal poisoning);
Glomerular - nephrotic syndrome, idiopathic, mesangial proliferation, focal sclerosis, glomerulonephritis, systemic diseases (lupus erythematosus), drugs, hypertension, diabetes mellitus, hemolytic uremic syndrome and other renal diseases.

Proteinuria may be divided into two categories:

of Glomerular Hematuria:
IgA nephropathy (Berger’s disease);
Thin glomerular basement membrane disease;
Hereditary nephritis (Alport’s syndrome).
Common Causes of Non-Glomerular Hematuria:
Upper Tract:
Urolithiasis;
Pyelonephritis;
Renal cell cancer;
Transitional cell carcinoma;
Urinary obstruction;
Benign hematuria
Lower Tract:
Bacterial cystitis;
Benign prostatic hyperplasia;
Transitional cell carcinoma;
Strenuous exercise (“marathon runner’s hematuria”);
Spurious hematuria (e.g. menses);
Instrumentation;
Benign hematuria

Qualitative changes of urine

RENAL

URETERAL

BLADDER

URETHRAL

to the naked eye.
Macroscopic hematuria can be divided into three types:
Initial Hematuria - bleeding that occurs at the start of urination. This could indicate a problem in the urethra in women or the prostate (in men).
Total Hematuria - bleeding that occurs while urinating is known as total hematuria. Men could experience total hematuria because of an enlarged prostrate. In women, vaginal bleeding during urination could be an indication of an infection in the bladder, ureter or kidneys.
Terminal Hematuria - bleeding after urination in men and women. Blood after urination in women is usually indicative of a bladder infection. Men can also experience terminal hematuria because of prostate diseases.

Haematuria is most usefully divided into:

of leukocytes in urine

Usually, the WBC's in urine are granulocytes.
The common diseases that may result to the presence of leukocytes in urine:
Urinary tract infection;
Cystitis – is the inflammation of the bladder (the infection has made its way from the urethra to the bladder, spreading the infection and damaging parts of the kidneys).
Pyelonephritis –is case, the infection has affected not only the urethra and the bladder, but also the kidneys.

kidney pathology (acute diffuse proliferative postinfectious GN, membranoproliferative GN, rapid progressive GN, lipoid nephrosis, focal segmental sclerosis, membranous glomerulopathy, IgA nephropathy, chronic glomerulonephritis);
2. Secondary - are caused by other organs and systems pathology or systemic diseases: (SLE, diabetes mellitus, amyloidosis, Henoch-Schenlein purpura, bacterial endocarditis);
3. Hereditary disorders - Alport syndrome, thin membrane disease etc.
Histopathological (patterns established on light microscopy):
Proliferative and nonproliferative variants are possible.
Membranous;
Mesangiocapillary;
Focal segmental glomerulosclerosis etc.
Etiological:
Inflammatory - the dominant aetiological agent for GN are bacteria, viruses, parasites;
Noninflammatory – immunopathological;
Idiopathic.

inflammation process leads to:
- decreased glomerular perfusion,
- retention of salt and water
- potential development of hypertension and edema.
Acute Poststreptococcal Glomerulonephritis (APSGN):
- is clearly the most frequent form of acute postinfectious glomerulonephritis;
- the clinical syndrome is often regarded as the prototype of the acute nephritic syndrome;
- Group A I²-hemolytic streptococcus serologic testing confirms recent infection (pharyngitis or pyoderma).

(5 - 15 years) and is more common in boys.
Patients are usually afebrile with a latency period following pharyngitis of 1 to 2 weeks and 3 to 6 weeks after a skin infection.
The most common presenting features are edema and gross hematuria. Essentially all the patients have microhematuria. The urine often has a color, described as smoky, cola-colored, or tea-colored.
Hypertension is common but is usually mild to moderate; rarely, hypertensive encephalopathy has been reported.
Nephritic syndrome is a typical manifestation of APSGN.
Fewer than 5% of patients develop nephrotic syndrome with significant proteinuria and a slightly depressed serum albumin level.

be microscopic or macroscopic. Podocytes develop large pores which allow blood and protein through.
Proteinuria - small amount, < 3.5 g/24 hr).
Hypertension is generally mild.
Oedema is usually mild and results from sodium and water retention.
Oliguria (low urine volume <300ml/day due to renal function been poor).
Red cell casts

Causes of Acute Nephritis:
I. Primary Glomerulonephritis - acute GN (post-streptococcal, non-streptococcal, rapidly progressive GN, membrano-proliferative GN, focal GN, IgA nephropathy).
II. Systemic Disease (SLE, polyarteritis nodosa, Wegener's granulomatosis, Henoch-Schonlein purpura, cryoglobulinaemia).

pathogenesis and characterized by clinical findings of:
Massive proteinuria (>3.5g in 24hrs, urine looks frothy), mostly consists of loss of albumin.
Hypoalbuminemia (albumin is lost in the urine due to gaps in podocytes allowing proteins to escape).
Oedema - is usually peripheral (swelling around ankles & eyes) due to:
loss of albumin and intravascular oncotic pressure decreasing;
sodium and water retention (secondary hyperaldosteronism, but osmotic pressure of blood is decreased);
increase of hydrodynamic intravascular pressure and vessels permobility (fluid moves out of vessels);
Hyperlipidemia/hyperlipiduria is caused by:
Hypoproteinemia stimulates protein synthesis in the liver, resulting in the overproduction of lipoproteins;
Lipid catabolism is decreased due to lower levels of lipoprotein lipase.
Hyperlipiduria is due to hyperlipidemia.

in children);
Membranous GN (most common in adults);
Membranoproliferative GN;
Focal GN;
IgA Nephropathy
II. Systemic Disease (diabetes mellitus, amyloidosis, SLE)
III. Systemic Infections:
Viral infections (HBV, HCV, HIV);
Bacterial infections (Bacterial endocarditis, syphilis, leprosy);
Protozoa and parasites (P. falciparum malaria, filariasis)
IV. Hypersensitivity Reactions:
Drugs (penicillamine, tolbutamide, heroin addiction);
Bee stings, snake bite, poison ivy
V. Malignancy (carcinomas, myeloma, Hodgkin's disease)
VI. Pregnancy (toxaemia of pregnancy)
VII Circulator Disturbances (renal vein thrombosis, constrictive pericarditis)
VIII. Hereditary Disease (Alport's disease, nail-patella syndrome)

function.
When less than 10% of renal function remains, this is termed end-stage renal failure (ESRF).
Renal failure may be:
- acute as usual is reversible process;
- chronic is termed end-stage renal failure (ESRF).

Acute renal failure (ARF) is an abrupt reduction in renal function with elevation of Blood Urea Nitrogen (BUN) and plasma creatinine levels, usually associated with oliguria (urine output of less than 30 ml/hr or less than 400 ml/day), although urine output may be normal or increased.

- is caused by impaired renal blood flow.
The GFR declines because of the decrease in filtration
pressure. Poor perfusion can result from hypotension,
renal vasoconstriction,, hypovolemia, hemorrhage,
or inadequate cardiac output.

Intra-renal - may result from pre-renal acute renal
failure (e.g., acute tubular necrosis or cortical necrosis)
or many other diseases, including acute glomerulonephritis,
malignant hypertension, disseminated intravascular
coagulation, and renal vasculitis.

Post-renal - usually occurs with bilaterally urinary tract
obstruction (e.g., bladder outlet obstruction,
prostatic hypertrophy, or bilateral ureteral
obstruction). Several hours of anuria with flank
pain followed by polyuria is a characteristic
finding. This type of renal failure can occur
after diagnostic catheterization of the ureters.

syndrome of renal failure and includes elevated blood urea and creatinine levels accompanied by fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes. Usually develops when the creatinine clearance falls to less than 10 mL/min.
Azotemia means increased serum urea levels and frequently increased creatinine levels as well. Renal failure causes azotemia.
Both azotemia and uremia indicate an accumulation of nitrogenous waste products in the blood.

intracellular K+
Increased levels of bioactive substances normally cleared renally (hormones)
Decreased levels of hormones and other mediators prodesed by the kidney
Decrease basal body temperature
Diminished lipoprotein lipase activity

skin
2. Cardiac manifestations - uremic pericarditis
3. Neurological manifestations - peripheral neuropathy
4. Pulmonary complications - pneumonitis and hemorrhage
5. Hematopoietic manifestations - anemia, bleeding diathesis
6. Skeletal abnormalities - renal osteodystrophy (secondary hyperparathyroidism)
7. Other metabolic imbalances