Download RENAL SYNDROMES

Main kidney syndromes
Renal diseases
RENAL SYNDROMES
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URINARY SYNDROME
NEPHROTIC SYNDROME
NEPHRITIC SYNDROME
ACUTE RENAL FAILURE
CHRONIC RENAL FAILURE
TUBULAR DISORDERS
HYPERTENSION
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Urinary syndrome
Clinical manifestation: latent course, no
complaints.
Urine tests
• Hematuria (commonly microhematuria)
• Leucocyturia
• Proteinuria (< 3 g/24 h)
Nephritic syndrome
• Etiology :
 Infection
 Vaccinations
 Systemic diseases
• Clinical manifestations
edema (face, eye lids)
oliguria
Hypertension
Proteinuria, hematuria («meat slops»)
± lung edema, acute renal failure
Diagnostic criteria of nephrotic syndrome
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Massive proteinuria (>3.5 g/24 h)
Hypoalbuminuria (< 35 g/l)
Disproteinemia (hyper-α2-globulinemia)
Dislipidemia
Edema (due to  of serum oncotic pressure
and retention of Na )
COMMOM CAUSES OF NEPHROTIC SYNDROME
Non-inflammatory glomerulonephritis
Minimal change nephropathy
Focal and segmental glomerulosclerosis (FSGS)
Membranous nephropathy
Proliferative/inflammatory glomerulonephritis
Mesangiocapillary glomerulonephritis (MCGN)
Other “subacute” proliferative nephritis
Systemic lipus erythematosus (SLE) (with a variety of
histopathological types)
Systemic diseases
Diabetic nephropathy
Amyloidosis
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CONSEQUENCES AND COMPLICATIONS OF
NEPHROTIC SYNDROME
Edema
Caused by avid sodium retention and hypoalbuminemia
Hypercoagulability
Presumed relative loss of inhibitors of coagulation
Venous thromboembolism is common and sometimes fatal
Hypercholesterolemia
High rate of arterial occlusions and disease
Infection
Especially by pneumococci
Associated with hypogammaglobulinemia
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Hypertensive syndrome
• Patogenesis : retention of Na and water due to
activation of renin-angiotensin-aldosteron system
(RAAS) and depression of prostaglandin-callecrein
system function.
• Clinical manifestation: depends on degree of BP
elevation and damage of cardiovascular system
Changes in urine appears before increase of BP and
usually are moderate
Hypertensive syndrome
• May be detected in:
acute glomerulonephritis
acutely progressive (crescent) GN
hypertensive and mixed GN
chronic pyelonephritis
chronic kidney failure
renal artery stenosis
Uncommon in latent course of chronic GN and chronic
interstitial nephritis
Tubular abnormalitis
Etiology : kidney congenital diseases, pyelonephritis,
interstitial nephritis, autoimmune diseases, tumors.
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Polyuria
Nocturia
< of urine density
Nephrogenic osteopathy
Electrolytes disorders
Glucosuria
Acidosis
Normal GFR
ACUTE RENAL FAILURE (ARF)
Deterioration in renal funcction manifestated by an
acute rise in serum creatinine and blood urea
nitrogen caused by inability to clear water,
electrolytes, and nitrogenous wastes, occurring over
hours to days/
• Prerenal: reduction in effective circulating volume
and renal perfusion or bilateral renal artery
occlusion
• Intrarenal: vascular, glomerular or tubular injuries
• Postrenal: obstruction of urinary tract or bilateral
renal veins
ACUTE RENAL FAILURE
Risk factors
• Age (newborns, pregnancy, labor, >60 years)
• Metabolic abnormalities (gout, atherosclerosis, diabetes)
• Hemodynamic (heart failure, liver cirrhosis)
• Drugs (sulfanilamide, antibiotics, ACE inhibitors, contrast
nephropathy)
• Toxins (alcohol, narcotics)
• Trauma (multiple traumas, massive burns, heart surgery)
• Renal causes (urinary tract obstruction, nephrotic
syndrome, gestosis, chronic renal failure)
Prerenal ARF
• Ischemic kidney
1. Decreased cardiac output (cardiogenic shock,
congestive heart failure, lung embolism)
2. Vasodilation (anaphylactic shock, sepsis,
drug indused hypotension)
3. Volume depletion (bleeding, diarrhea,
vomiting, polyuria, reduction of effective circulation
volume due to hypoalbuminemia)
4. Other reasons for GFR (hypercalciumemia,
hepatorenal syndrome)
Intrarenal ARF
• Exogenous intoxication
(poisons, snake bites and stings, drugs)
• Acute infection-toxic kidney (hemorrhagic fever,
leptospirosis, acute pyelonephritis)
• Injury of renal vessels
(hemolitico-uremic syndrome, scleroderma, thromboembolic and
atheroembolic disease, systemic vasculitis, acute
glomerulonephritis, interstitial nephritis, acute tubular necrosis,
contrast nephropathy)
• Kidneys traumas
• Postischemic ARF
• Intratubular blok
(pathologic cylinders, cristalls)
Postrenal ARF
• Urinary tract and renal veins obstruction
(nephrolithiasis, tumors, retroperitonal
fibrosis, renal necrotic papillitis, prostatic
hypertrophy, renal vein thrombosis)
• Urinary retention
(diabetes, spinal cord injury, M-cholinergic
antagonists and ganglionic blockers)
Clinical manifestation of ARF
• Initial stage (I):
clinical manifestation of situation leading to ARF
• Oligouria or anuria (II):
acute development of oligouria or anuria, vomiting,
impairment of consciousness, edema, lung and brain
edema,  of urea, creatinine, potassium, GFR, metabolic
acidosis
• Restoration of diuresis (III): polyuria, увеличивается
количество мочи до степени полиурии,  of urea,
creatinine, potassium, sodium
• Recovery (IV): takes 6-12 monthes
Chronic renal failure
• Constant and progressive decrease of all
kidney functions
• Kidneys are incompetent to support normal
homeostasis
Causes of chronic renal failure
Chronic glomerulonphritis
Systemic hypertension
Diabetes mellitus with nephropathy
Chronic obstructive uropathy
Polycystic of the kidneys
Analgesic nephropathy
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Signs of chronic renal failure
Sallow complection
Anaemia (normocytic, normochromic)
Uraemic fetor
Deep acidotic breathing (Kussmaul respiration)
Hypertension
Mental clouding
Uraemic encephalopathy (flapping tremor)
Pleural and pericardial effusion
Pericardial rub (pericarditis)
Evidence of fluid overload or depletion
Renal masses (polycystic kidneys)
Large bladder (chronic bladder outlet obstruction)
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Mechanisms of progression
• Activity of disease
• hemodinamic
– Hyperfiltration and intraglomerular hypertension
– Systemic hypertension
• Metabolic
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↑phosphorus
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↑ calcium
↑ lipids
↑ glucose
↑ uric acid
• Provoking factors
infections, UT obstruction, pregnancy, allergic reactions,
nephrotoxic drugs, hypovolemia, dehydration, bleeding
REVERSIBLE FACTORS IN CHRONIC RENAL
FAILURE
Hypertension
Reduced renal perfusion
Renal artery stenosis
Hypotension due to drug treatment
Sodium and water depletion
Decreased cardiac output
Urinary tract obstruction
Urinary tract infection
Other infections: increased catabolism and urea
production
Nephrotoxic medications
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Conservative treatment of CRF
• Low-protein diet, control of phosphorus and potassium
according to level of GFR
• Control of BP (target BP < 130/80 mm Hg)
• Control of water-salt and acid-base balance
• Correction of renal anemia (erythropoetine)
• Prophylaxis of hypertireoidism
• Excretion of nitrogen rests via GIT
• Treatment of infectious complications
• Decrease of cardiovascular risk
Cardiovascular risk
• Cardiovascular risk in patients with CRF is 15-20
times higher then in general population
• 40% patients starting dialysis have features of
ischemic heart disease
Markers of activity of renal disease
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Increase of proteinuria
Increase of hematuria
Sudden increase of BP
Rapid increase of creatinin
Rapid decrease of GFR
Increase of EST
Hyper-α2 or gammaglobulinemia
• Intravascular blood coagulation
Glomerulonephritis
Provoking factors
• Infection
(streptococci, staphylococci, tuberculosis, luis, hepatitis B and C, other viruses,
malaria, ricketsiosis)
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Vacination
Systemic diseases, tumors
Concomitant diseases
Drugs
Narcotics
Allergic reactions
Toxic substances
Radiation
Overcooling
Clinical classification of GN
• Acute
• Rapidly progressive
• Chronic
- latent
- latent with hematuria
- nephrotic
- hypertensive
- combined
Acute GN
• Develops in 10-20 days after infection or injury
(ß-hemolitic streptococcus, gr. A)
• Nephritic syndrome - edema, oliguria BP,
hematuria, proteinuria
• In some patients - lung edema, eclampcia, ARF
•  АSLO
• In case of cyclic course recovery in 2 -3 weeks
• Morphology: diffuse proliferative GN
Clinical case 1
• Genesis of nephrotic syndrome
Drug-induced?
Secondary lues?
• Treatment
Exclude the intake of carbamazepine and
phenobarbital?
Treatment of lues?
Clinical case 1
• Diagnosis
Secondary lues. Acute glomerulonephritis with
nephrotic syndrome. Preserved renal function.
• Morphology
Most common membranose nephropathy with
deposits of Ig G, Ig M and Trepanema pallidum on
basal membran
• Catamnesis
In 6 months there were no signs of kidney damage
Rapidly progressive GN
• Nephritic and/or nephrotic syndrome,  BP
• Rapid developpment of renal failure (dubbling of
creatinine every 3 months)
• Without treatment death in 1-2 years
• Morphology: creschendic nephritis with “demilunes”
• Etiology: systemic vasculitis, systemic diseases, hepatitis C
Latent chronic GN
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Most common form (44%)
Isolated urinary syndrome
Rarely  BP
10-years survival 88%
• Morphology: mesangioproliferative GN
Hematuric chronic GN
• Episodes of micro- and macrohematuria after
flu and respiratory viral infections
• More common in males
•  of Ig A in blood
• In most cases – benign course
• Morphology: mesangioproliferative GN
• Berge disease, alcoholic damage of kidneys
Nephrotic GN
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Course with exacerbations
Edema
Proteinuria > 3,5 g/24 h
Hypoalbuminuria < 35 g/l
↑of α-2 and γ-globulines
Hypercholesterolemia
Morphology: minimal changes, membranous and
mesangioproliferative GN, focal segmental
glomerulosclerosis
• Develops in infective endocarditis, systemic diseases, drug
induced damage, Alport’s syndrome
Hypertensive GN
• ↑BP, sometimes malignant
• Urinary syndrome (proteinuria < 1g/24 h)
• Differential diagnosis with renovascular
hypertension, Conn syndrome,
pheochromocytoma, essential hypertension,
chronic pyelonephritis
Combined GN
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Nephrotic syndrome
Hypertension
Chronic renal failure develops in2-3 years
Morphology: membranoproliferative GN, focal segmental
glomerulosclerosis
• Diseases: systemic lupus erythematosus, systemic
vasculitis
• Differential diagnosis with renal vein thrombosis, acute
interstitial nephritis, scleromermic kidney
Treatment of glomerulonephritis
• If possible detect the etiologic factor and eliminate it
• Decrease the activity of the processes
• Stabilize the course of disease and decrease the temp of
progression (if possible – achieve the involution of disease)
Treatment of glomerulonephritis
Etiologic treatment
- Antibiotics in post-strepthococcal GN and infective
endocarditis
- Specific treatment of GN associated with lues, malaria,
tuberculosis, viral infections
- Effective treatment of tumors in case of paraneoplastic
nephritis
- Exclusion of drugs in drug induced nephritis
- Refuse of alcohol in alcoholic nephritis
- Exclusion of allergic factor in atopic nephritis
Treatment of glomerulonephritis
Pathogenic treatment
Immunosupression
Corticosteroids
Cytostatics
nonselective
alkalizing: cyclophosphamide, clorbutin
antimetabolic: azathioprine, metatrexat
selective
-cyclosporine А
-tacrolimus
-micofenolat mofetil
Monoclonal antibodys (?)
Indications for corticosteroids
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Nephrotic syndrome in minimal changes disease
Rapidly progressive GN
Exacerbation of GN in systemic diseases
Acute GN with long lasting nephrotic syndrome and
increase of creatinin
• Exacerbation of GN with first episode of kidney
failure and/or nephrotic syndrome
• Drug induced GN or interstitial nephritis
Mechanism of corticosteroids action
• Redistribution of inflammatory and immune
system cells in blood flow, prevention of their
migration in the kidney tissue
• Depression of inflammatory cells proliferation
and production of inflammatory mediators
Methods of steroid therapy
• Prednisolone 1 mg/kg (but not more than 80 mg)
every day
• Dabbled dose of prednisolone every other day
- ↓risk of adrenocortical insufficiency
- ↓risk of infective complications
• Pulse therapy - IV infusion of very high doses of
prednisolone (1000 mg) during 3 days every month
Complications of corticosteroid therapy
• CNS - psychosis
• Bones and muscles
- osteoporosis
- myopathy
• Eyes – glaucoma, cataract
• GIT – peptic ulcer, pancreatitis
• Cardiovascular system – AH, HF, cardiopathy
• Immune system – immunosuppression
• Endocrine system and metabolic changes
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Steroid diabetes
Ameorrhea
Cushing syndrome
Fatty liver
Complications of corticosteroid therapy
• Endocrine system and metabolic changes
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↑of glucose level (steroid diabetes)
Dislipidemia
Cushing’s syndrome
Fatty liver
P-Ca metabolism abnormalities
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Mechanism of cytostatics agents
action
• Antimetabolites – impair basic nitrogens synthesis
• Alkylating agents – suppress the information
reading from DNA and damage the protein
synthesis in ribosomes
• Cyclosporine А – decrease the activity of Т-helpers,
proliferation of В-lymphocytes, production of IL-2
and other cytokines
Indications for cytostatics
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Acutely progressive GN
Exacerbation of GN in SLE
High activity of GN
Recurrent and persisting nephrotic syndrome
Steroid sensitivity and resistency
Complications of cytostatic therapy
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Decrease of thrombocytes and leucocytes
Infections
Gastro-intestinal disorders
Liver damage
Amenorrhea
Alopecia
Cystitis
Teratogenicity
Cancer genesis
Control of leucocytes is obligatory
(neutrophils - > 1500!)
Influence on non-immune mechanisms of
GN progression
• ACE-inhibitors and angiotensin II receptor
blockers
• Anticoagulants and antiaggregants
heparin
dipiridamol
• Antihiperlipidemic drugs
CLINICAL PRESENTATION OF URINARY
TRACT INFECTION
Asymptomatic bacteriuria
Symptomatic acute urethritis and cystitis
Acute prostatitis
Acute pyelonephritis
Septicaemia (usually Gramm-negative
bacteria)
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UNCOMPLICATED AND COMPLICATED URINARY
TRACT INFECTION
Uncomplicated
Anatomically and physiologically normal urinal tract
Normal renal function
No associated disorder which impairs defense mechanisms
Complicated
Abnormal urinary tract, e.g. obstruction, calculi,
vesicoureteric reflux, neurological abnormality, in-dwelling
catheter, chronic prostatitis, cystic kidney, analgesic
nephropathy, renal scarring
Impaired renal function
Associated disorder which impairs defense mechanisms (e.g.
diabetes mellitus, immunosuppressive therapy)
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FACTORS WHICH LIMIT MULTIPLICATION IN THE
URINARY TRACT
A high rate of urine flow
Regular complete bladder emptying
Urinary glucosaminoglycans (Tamm - Horsfall
mucoprotein) which may bind to E.coli, thus
preventing their attachment to urothelium
Mucosal defences: this surface layer on
glucosaminoglycans, secretion of IgA and IgG, mucosal
phagocytosis
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Investigation of patients with acute urinary tract
infection
Investigation
Indications
Culture of MSU or urine
obtained by suprapubic
aspiration
Microscopic examination
of urine for white cells,
red cells and casts
Dipstick examination of
urine for blood, protein
and glucose
Full blood count
All patients
Plasma urea, electrolytes,
creatinine
All patients
All patients
Infants; children; acute
pyelonephritis or
prostatitis
Infants; children; acute
pyelonephritis; recurrent
UTI
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Investigation of patients with acute urinary tract infection
Blood culture
Pelvic examenation
Intravenous urography
(IVU) including film of
bladder after voiding, to
identify physiological and
anatomical abnormalities
Renal ultrasonography
Micturating cystourethrography (MCU) to
identify and quantitate
vesico-ureteric reflux and
disturbed bladder emptying
Cystoscopy
Fever, rigors or evidence of
septic shock
Women with recurrent UTI
Infants; children
Men after single UTI
Women who (1) have acute
pyelonephritis; (2) have
recurrent UTI after urinary
tract treatment; (3) have had
UTI or covert bacteriuria in
pregnancy (IVU 6 weeks
after delivery)
Alternative to IVU to identify
obstruction, cysts, calculi
Infants; children with
abnormal IVU; any patient
thought to have a
disturbance of bladder
emptying
Patients with chronic
haematuria; patients with a
suspected bladder lesion
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