CHAPTER 5

PRIVATE NEPHROLOGY

5.1 PYELONEPHRITIS
This is a non-specific inflammatory process with a predominant lesion of the interstitial tissue of the kidneys
and their Cup-pelvic system. The infection gets into the renal pelvis and interstitial tissue urinogenous (via
urinary tract) or hematogenous route (via blood) way.
Most often, the pathogen is E. coli. In addition, the pathogen can be streptococci, staphylococci, and other
bacteria.
Risk factors may include:
• Heredity;
• Violation of urodynamics (pielavesi, pyelolithotomy refluxes) wide, short female urethra, nephroptosis;
• Dysbacteriosis of the urethra;
* Medical urological manipulations;
* Hypothermia, inflammatory diseases of the genital area;
• Diabetes.
Classification
1. Acute-serous or purulent. Within 6 months, all symptoms disappear,
Chronic-latent or recurrent
2. Primary-developed in a healthy kidney without disruption
urodynamics,
Secondary – developed against the background of kidney disease, abnormalities of the kidneys and/or
urinary tract, or urodynamic disorders (ureter stricture, benign prostatic hyperplasia, urolithiasis, urinary
tract atony, reflux dyskinesia).
3. Phases of chronic recurrent pyelonephritis: exacerbation (active pyelonephritis), remission (inactive
pyelonephritis)
4. Localization: one-way (rarely), two-way
5. With or without hypertension
6. Uncomplicated (usually in outpatient patients), complicated by kidney abscess, carbuncle,
paranephritis, sepsis, during catheterization, urodynamic disorders (urolithiasis, polycystic kidney disease,
benign prostatic hyperplasia), immunodeficiency States (DM. Neutropenia)
7. Renal function was preserved, broken, chronic renal failure.
There are special clinical forms:
* Pyelonephritis of newborns and children
* Pyelonephritis of the elderly and senile age
* Gestational pyelonephritis – pregnant, birth, postpartum
* Calculous pyelonephritis
* Pyelonephritis in patients with diabetes
• Other
Acute pyelonephritis
THE MAIN SYNDROMES :
1. Pain syndrome
2. Urinary syndrome
- proteinuria (traces of protein up to 1.0 g / l);
lakeshore (significant up to pyuria):
- bacteriuria (100 thousand microbial bodies / ml or more).
3. Urination disorder syndrome
4. Intoxication-inflammatory

DIAGNOSTICS: General urinalysis, urinalysis for flora, determination of blood elements (Necheporenko,
Amburge), Zimnitsky's sample, kidney ultrasound, overview radiography of the urinary system, in/in
urography, chromocystoscopy.

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 Chronic pyelonephritis
Causes: incurable acute pyelonephritis or primary chronic, i.e. can occur without acute events from the
beginning of the disease. In most patients, chronic pyelonephritis occurs in childhood, especially in girls. In
1 / 3 patients with normal examination, it is not possible to identify undoubted signs of pyelonephritis.
Clinical and laboratory signs are expressed in the period of exacerbation and scanty in the remission phase.
Exacerbation of chronic pyelonephritis occurs in the type of acute pyelonephritis.
THE MAIN SYNDROMES:
1. Pain syndrome
2. Urinary syndrome
- proteinuria up to 1.0 g / l
- leukocyturia
- bacteriuria
3. Syndrome of arterial hypertension with a high diastolic pressure (180/115 - 220/140 mm Hg.art.).
4. Subsequently, CPN (chronic kidney failure) develops.
5 Additional syndrome - intoxication-inflammatory.
DIAGNOSTICS: General urinalysis, urinalysis for flora, determination of blood elements (Necheporenko,
Amburge), Zimnitsky test, Rehberg test, kidney ultrasound, overview radiography of the urinary system, in /
in urography, chromocystoscopy.
EXAMPLE OF DIAGNOSIS FORMULATION:
Primary chronic bilateral pyelonephritis, relapsing course, aggravation of chronic renal failure 0.

5.2 GLOMERULONEPHRITIS – is an immuno-inflammatory kidney disease with predominant

glomerular damage, but involving both tubules and interstitial (interstitial) tissue in the pathological process.
The process is diffuse.
Glomerulonephritis can be primary (idiopathic), the clinical manifestations of which are limited only by the
kidneys, or secondary-part of a systemic disease (more often SLE or vasquita)

Acute glomerulonephritis
Classification of OGN (TAREEV 1983)
According to the etiology:
* Infectious-immune
a) bacterial (b-hemolytic Streptococcus)
b) viral (hepatitis B, rubella, infectious mononucleosis, herpes, adenovirus)
C) parasitic (leptospirosis, rickettsiosis, brucellosis)
d) fungal
* Allergic (post-vaccination 70-75% FIRE after the 2nd-3rd vaccination).
* Toxic (chemicals) plant pollen, insect venom, alcohol.
• Drug
* Hemodynamic (on the background of NC, crash syndrome).
* Mixed etiology
• Unspecified
By pathogenesis
• Autoimmune
autoantibodies interact with an antigen - a protein of the glomerular basal membrane-to form a CEC with
deposits on the basal membrane, causing damage to it.
* Immunocomplex 60-80%.
Antibodies are combined with extrapubular antigen (including Streptococcus) complexes are formed And
deposited on the basal membrane of the glomerulus, or in the mesangia
* Non-immune
violation of renal hemodynamics due to renovascular lesions (congenital, acquired), lead to a violation of
blood microcirculation and rheology as a result of increased V / vascular coagulation in glomerular
capillaries, platelet aggregation and loss of fibrin leading to thrombosis and obturation of the capillary
lumen.

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The clinical course
* Monosymptomatic
• Polysiphonia - classic or cyclic option
* Nephrotic variant (prolonged course of outcome in CGN).
* Latent - there are no extrarenal signs (edema, hypertension), late access to medical care
Diagnostic sign of latent options - urinary syndrome (microproteinuria and microga Mature).
By period
* Pre-critical
* Expanded (nephritic)
• Outcomes:
a) full recovery from 2-4 weeks, up to 3 months, up to 1.5 years;
b) recovery with a "defect" (unstable proteinuria, red blood cells).
Reason: late diagnosis, inadequate therapy;
C) recovery
g) the transition to CGN
e) lethality
Complications:
* encephalopathy (angiospastic hypertension)
* hemorrhages (in the vital centers of the brain)
• brain edema
• ascites
• hydrothorax
• hydroperiod
• anasarca
• eclampsia
hronic glomerulonephritis

CLASSIFICATION of HGN 1972 (TAREEV E. I.) (MOSCOW-great BRITAIN)

I. Onset: 1) primary-chronic (without acute onset)
2) secondary-chronic (after OGN)
II. According to the etiology:
a) primary:
• infectious;
* non-infectious (medicinal, alcoholic, with serum
diseases, paraneoplastic);
* genetically determined (Berger's disease, etc.).
b) secondary:
• systemic diseases (PM, RA, SLE, DM, disease Henoch-Schonlein purpura, tumors);
• special form:
- post-eclamptic
- genetic (familial, Mediterranean fever)
- radiation
- drug.
III. By pathogenesis:
* autoimmune (Berger's disease)
• immune
• hypocomplementemia
* non-immune (alcoholic).
IV. On morphology (who experts 1978 London):
* Membranous glomerulonephritis (carcinomas, HCG, SLE)
* Mesangial GN:
- mesangioproliferative; (HG B, b-NY Crohn's, spondyloarthritis)
– mesangiocapillary;(hepatitis C, SLE, bacterial infections)

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– lobular.
* Lipoid nephrosis (idiopathic; mainly in Pediatrics) with minimal changes.(ARI, NSAIDs, DM,
vaccination)
* Focal sclerosing (focal segmental glomerular hyalinosis).(HIV, anemia, transplant rejection, idiopathic)
* Fibroplastic GN (outcome of glomerulopathies)
* Secondary-wrinkled kidney
Table 4
V. Clinical variants of CGN
Clinical Clinical manifestations
variants of CGN
Latent (often occurs) Proteinuria up to 3 g / day, hematuria 5-10 to 50 red blood cells in the field of vision,
Minor hypertension
It can have a very long course (10-20 years or more), but later still leads to the
development of uremia
Hematuric Macrogematuria without significant proteinuria and common symptoms
(hypertension, edema).
Nephrotic Massive proteinuria more than 3.5 g / day, hyperproteinemia, dysproteinemia,
hypercholesterolemia, edema, in the urine, hyaline, granular and waxy cylinders
Hypertonic Hypertonic syndrome (high persistent hypertension), minor urinary syndrome
Mixed Combination of nephrotic and hypertensive syndromes. Steadily progressing course.

All forms of chronic glomerulonephritis can periodically give relapses, very similar or completely repeating
the picture of acute diffuse glomerulonephritis. Most often, exacerbations are observed in autumn and spring
and occur 1-2 days after the impact of the stimulus, most often streptococcal infection. With any course of
chronic diffuse glomerulonephritis, it passes into its final stage-the second-wrinkled kidney (CPN).
VI. By CGN phases:
* Exacerbation (active phase, relapse) - the appearance of nephritic or nephrotic syndrome;
* Remission (inactive phase) - improvement or normalization of extrarenal manifestations (edema,
hypertension), kidney function, and changes in urine.
VII. Adrift:
* fast-progressing
* slow-progressing
* recurrent (indicating the acute phase, remission)
VIII. Stage and phase of CPN.
Determined by the level of creatinine and glomerular filtration.
COMPLICATIONS OF CGN.
– HPN.
- Infectious or purulent processes (pneumonia, abscess, phlegmon).
– Cerebral stroke.
– Heart attack
– Hemorrhagic syndrome.
- Pulmonary edema (nephrotic syndrome)
– Cardio-vascular insufficiency.
– Anemia.
SYNDROMES:
1 Urinary syndrome (proteinuria, hematuria, cylindruria)
2. Nephrotic syndrome.
3. Syndrome of arterial hypertension
4. Nephritic syndrome

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DIAGNOSTICS: General urine analysis, to determine the form of blood elements (Nechiporenko,
Amburge), Zimnitsky's sample, Rehberg's sample, biochemical analysis (creatinine, urea, residual nitrogen,
potassium), kidney ultrasound, overview radiography of the urinary system, in/in urography, kidney biopsy.

EXAMPLE OF DIAGNOSIS FORMULATION:

Chronic glomerulonephritis, mixed form, active phase, slowly progressive course. CPN 1 art.

5.3 KIDNEY STONE DISEASE

A chronic disease characterized by changes in the kidneys and urinary tract with the formation of urinary
stones (concretions) in them.
Urinary stones are formed from urinary salts and can be of a very different composition: urates, oxalates,
phosphates, mixed, etc.They can be single or multiple, ranging in size from a grain of sand to an egg.
The formation of various stones is promoted by an oversaturation of the urine with salts (excessive excretion
of salts) due to certain metabolic disorders or low diuresis, as well as their poor distribution in the urine,
urinary tract infection and alimentary factor. In the acidic reaction of urine, oxalate-calcium, urate and
cystine stones are formed, in the alkaline reaction-stones consisting of phosphate and calcium carbonate,
tripelphosphates (struvites).
RISK FACTOR:
•Family history,
• History of ICD episodes,
* Persons exposed to increased physical activity
* Persons whose work is associated with long-term hyperthermia (divers)
• Some diseases, predisposing to the development of ICD (polycystic kidney disease, sarcoidosis,
generartions),
* Increased fluid loss,
• Admission of poorly soluble drugs
SYNDROMES:

1. Pain syndrome
2 Urinary syndrome-inorganic urine sediment ( urates, oxalates, phosphates; fresh red blood cells; in
inflammation-white blood cells;
3. Urination disorder syndrome
4. Intoxication-inflammatory

COMPLICATIONS of NEPHROLITHIASIS — acute and chronic pyelonephritis, hydronephrosis, anuria,

due to obturation of the urinary tract on both sides, urosepsis.

5.4 AMYLOIDOSIS
Amyloidosis is most often a systemic disease, which is based on complex metabolic changes that lead to the
formation and loss of a special substance in the tissues, called R. Virchov amyloid.
Allocate 1. PRIMARY AMYLOIDOSIS (sporadic cases of amyloidosis in the absence of a "causal"
disease), as well as hereditary (family), senile amyloidosis.
2. SECONDARY AMYLOIDOSIS
Development and progression is associated with a number of chronic
diseases (tuberculosis, bronchiectasis, chronic lung abscesses, osteomyelitis, rheumatoid arthritis, ulcerative
colitis, lymphogranulomatosis).
STAGES OF SECONDARY AMYLOIDOSIS:
1. Latent (preclinical, dysproteinemias):
* No clinic;
* Dysproteinemia (increased alpha-2 and gamma globulins, increased ESR);
• Urinary syndrome – microproteinuria (non-permanent).
2. Proteinuric stage (from several months to 5-10 years).
* Dysproteinemia,

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* Increased ESR.
• Urinary syndrome :
- proteinuria constant up to 1.0 g / l, rarely up to 2-ZG/l;
- minor erythrocyturia;
- cylindruria.
* Kidney function is not impaired.
3. Nephrotic stage.
• Nephrotic syndrome
4. Azotemic stage.
• Nephrotic syndrome.
* Chronic kidney failure syndrome.
Note: Among other manifestations of amyloidosis observed dysfunction of the cardiovascular system
(primarily in the form of hypotension, hypertension rarely, various violations conductivity and heart rhythm,
heart failure) and gastrointestinal tract (malabsorption syndrome). Often there is an increase in the liver and
spleen, sometimes without any signs of changes in their function.