glomerulonefritis skaidres Flashcards by lukas s

Secondary GN are divided into

Secondary GN:

Secondary GN after infective disease

Secondary GN after drugs or toxins

Secondary GN after systemic diseases:

· Goodpasture syndrome

-Vasculitis

· Cryoglobulinemia

-Lupus nefritis

- secondary GN after neoplasia

Other glomerulopathies with non-immunologic cause:

-DIabetes mellitus

Amyloidosis

Multiple myeloma

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Hystology of lupus nefritis

I -Normale

II - Mesangial GN

III - proliferative GN segmental and focal

IV - proliferative - diffuse GN

V - membraneous GN

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Lupus nefritis clinic

Clinica

Segni extrarenali del L.E.S.
Urinary anomalies

S. S. Nefritica; S. Nefrosica

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Lupus nefritis laboratory investgigations

less C3. ANA +, Ab>DNAs

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Vasculitis

Inflammatory conditions affecting the walls of blood vessels (mainly arterial)

Are classified according to the size of the vessels involved:
• Small arms (Glomerular Capillary type)-> Glomerulonephritis
• Medium and large caliber-renal Ischemia >
Ischemia renale

Vessel Vasculitis of small arms are divided into:

ANCA-positive

• ANCA-negative

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Hystology of ANCA-positive vasculitis. diseases and microscopy

(Granulomatosi di Wegener, Micropoliarterite, Malattia di Churg-Strauss)

Areas of fibrinoid necrosis in Glomerular Capillary Wall; semilunar

Granulomi

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ANCA-Positive vasculitis imunofluorescence

Negative; In some cases, deposits of Ig, C3 and fibrin

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ANCA-Positive vasculitis clinica

Flu Syndrome, arthralgia, purple, asthma

and hemoptysis (sometimes)

Rapidly progressive GN;

variable proteinuria and hematuria;

arterial hypertension

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Anca-positive laboratory exams

ANCA +: cANCA in GW;

pANCA in MPA. eosinofilin.

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Vasculitis anca-negative. diseases, their properties

Vasculiti ANCA-negative.

Henoch-shonlein purpura similar to GN mesangial.IgA more.

crioglobulinemia. similar to GN membranoproliferativa.more crioglobuline, less C4

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Functional alterations of diabetes

FUNCTIONAL ALTERATIONS
Glycosuria
Osmotic diuresis

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Gliucosuria

GLYCOSURIA

 is always a given pathological
secondary to an increase of filtered glucose load by increasing blood sugar
in the case of IRC the diabetes mellitus, glycosuria is reduced for the declineof Glomerular filtrate

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Osmotic diuresis

Glucose is not reabsorbed increases urinary osmolarity reducing the reabsorption of water and sodium (mostly) resulting polyuria, polydipsia hypotonic edeplezioneidro-salina

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Papillary necrosis

PAPILLARY NECROSIS
 Ischemic Infarction by one or more of the taste of one or both kidneys
 high incidence in diabetic patients for the frequent
combination of multiple causes of alteration of the spraying
Renal Medulla of the kidney (diabetic microangiopathy, airway infections
congenital obstructive urinary, drugs)
 The necrosata papilla may break causing a renal colic
 diagnosis relies on urografico

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DIABETIC NEPHROPATHY

DIABETIC NEPHROPATHY
Persistent and progressive alteration
of renal function caused by diabetes mellitus
 The necrosata papilla may break causing a renal colic

 diagnosis relies on urografico
in the absence of other causes of kidney damage
(Glomerulonephritis,pielonefriti, interstitial nephritis, etc.)

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pathogenesis of diabetic nephropathy

The pathogenesis of diabetic nephropathy is multifactorial
Are involved:
 genetic factors
 environmental factors (Smoking, Diet, physical activity)
 more renal Angiotensin II
-Systemic (hypertension)
-Intrarenali (AII, Glomerular Iperfiltrazione )
 Metabolic Factors (Hyperglycemia  AGEs)

Diabetic nephropathy stages

Latency (10-20 years after the onset of diabetes mellitus)
INCIPIENT NEPHROPATHY (1-5 years)
NEPHROPATHY FRANCA (5-15 years)

diagnosis of diabetic nephropathy

Diagnosis of diabetic nephropathy
The ability to diagnose diabetic nephropathy from pre-clinical phase is of

crucial importance in order to slow the progression.
FOLLOW UP OF PCS WITHOUT

DIABETIC PROTEINURIA
• Medical history, Review objective
• Laboratory tests (CL. creat., HbA1C,

Microalbuminuria)
• Eye Primer
• ECG, Echocardiogram, Doppler TSA and limbs
FOLLOW UP OF PCS WITH

DIABETIC PROTEINURIA
• Collection of diuresis of 12:0 am (Creatininuria, Proteinuria, Na + and K +)
• Renal Ultrasound with doppler study of renal vessels
Renal Biopsy

Prevention, theraphy of diabetic nephropathy

It requires a multidisciplinary approach and with the adoption of thenecessary therapy and periodic checks.
 LIFESTYLE CHANGES
(Smoking, diet, physical activity, self-monitoring blood glucose)
 HYPOGLYCEMIC THERAPY
(Target blood sugar: 80-120 mg/dl in fasting and 140-180 mg/dl 2:0
after meals; HbA1c) 7.0 <
 treatment of DYSLIPIDEMIA (statins)
 SUPPRESSION of RAS (ACE-I, etc.)
 HYPERTENSION THERAPY (130/80 <)

Hemodynamic changes during pregnancy

increase cardiac output
decrease peripheral Resistance
decrease blood pressure

75 mmHg nel II trimestre
85 mmHg nel III trimestre

Changes in renal function during pregnancy

Changes in renal function during pregnancy

increase of FPR
increase of GFR (40-50% at the end of the first trimester)
v.n. BUN = 8-12 mg/dl Creatinine = 0.4-0.8 mg/dl
decrease urinary excretion of Na + (900  retention mEq)
decrease urinary excretion of K +
increase of urinary excretion of glucose (0.5-1 g/12:0 am)
increase of urinary excretion of uric acid
increase of Proteinuria

Modification of Eq. electrolytic water in pregnancy

increase of total body Water (7-8 L)
increase of extra-cellular Volume (5-6 L)-> EDEMA
increase of plasma Volume (1-1.5 L)-> decrease of Htc, Proteins
decrease of plasma Osmolarity
Hyponatremia (for raising of stimulus threshold of ADH)
Respiratory alkalosis (progesterone stimulates the breathing Centre)

Renal diseases associated with pregnancy are:

Renal diseases associated with pregnancy are:
 ACUTE RENAL FAILURE
 URINARY TRACT INFECTIONS
 HYPERTENSION

Acute Renal Failure

which clinical traits are ARF specific during pregnancy:

Acute Renal Failure
 high incidence of ANGER during pregnancy for the existence of various
risk factors:
 Lability of hydro-electrolytic balance
 anatomical Modification
 Bleeding pre-and post-partum
Hypercoagulability

which clinical traits are ARF specific during pregnancy:

 ARF post-abortion
 acute cortical Necrosis

Urinary tract infections

**Urinary tract infections**  the incidence of UTI in pregnancy is only slightly higher than that of women of childbearing age  The eventuality that you establish pyelonephritis is very high  No fetotoxic effects drugs therapy ![]()

Hypertension in pregnancy

Hypertension in pregnancy CHRONIC HYPERTENSION  140/90 mmHg before pregnancy and/or before the TWENTIETH week ![]()

PRE-ECLAMPSIA/ECLAMPSIA after some week.

PRE-ECLAMPSIA/ECLAMPSIA After the TWENTIETH week • Ar 140/90 mmHg \> and/or increased PAS increase \> 30 mmHg and/orincreased \> PAD 15 mmHg • Proteinuria • Edema and/or rapid increase in body weight ![]()

Pre-eclampsia / Eclampsia detailed

 Occurs after the 20TH week of gestation  Complicates the 5-7% of pregnancies  is characterized by: IPERTENSIONEARTERIOSA PROTEINURIA EDEMA CONVULSIONS (ECLAMPSIA)  The detection of Edema and Proteinuria is not required for the purposes of diagnosis  In 20% of cases, despite eclamptica evolution PAD \< and/or 90 mmHg no proteinuria ![]()

Pre-eclampsia / Eclampsia part 2, complications.

 leading cause of maternal death during pregnancy  possible complications: • Cerebral hemorrhage • HELLP Syndrome (hemolysis, thrombocytopenia,  GOT, GPT) • Retinal detachment • Hepatic Rupture • Pulmonary Edema • CID • IRA • Untimely Detachment of the placenta • Fetal growth Retardation, intra-uterine death of fetus ![]()

Evolutionary form of pre-eclampsia

EVOLUTIONARY Forms • 110 mmHg \> 24h PAD after therapy • increase body weight • increased Creatinine, GOT, LDH, proteinuria • Signs of fetal distress • Abdominal pain • Visual disturbances, headache, Hyperreflexia, Clonus • Coagulopathy ![]()

AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE what kind of disease, it's genetics

AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE Hereditary disease (1 case every 400-1000 live births), with high penetrance (90-100%) but highly variable expressivity (Dx performed in less than 50% of patients). GENETICS • PKD1 gene mutation (chromosome 16) [86%-European data] • PKD2 gene mutation (chromosome 4) • TG737 gene mutation (chromosome?) ![]()

Renal manifestations of AD polycystyc kidney disease

RENAL MANIFESTATIONS bilaterally enlarged kidneys, to surface bernoccoluta; progressive replacement of Renal parenchyma by numerous cysts of size varies, generally rounded, filled with clear liquid, sometimes other dense, brownish-red or pioide. ![]()

Extra-renal manifestations of autosomal dominan policystic kidney disease

EXTRA-RENAL MANIFESTATIONS Liver cysts (40-60) Cerebral aneurysms (~ 20) Pancreatic cysts, spleen cells Ovarian cyst, thyroid, pituitary, testicular Valvulopatie (mitral prolapse, aortic, mitral low.) Inguinal hernias, hiatal Diverticulosis of colon ![]()

CLINICAL MANIFESTATIONS of extra-renal kidney disease autosomal dominant

**CLINICAL MANIFESTATIONS of extra-renal kidney disease autosomal dominant** Pain in side, abdominal pain (80) High blood pressure (50) Palpable abdominal masses, kidney Renal colic [clots, stones] (20) Headache Urinary infections (often charged high street) Hematuria (50-60) Proteinuria [1 g/12:0 am \<] (70-80) Inability to concentrate the urine (~ 100) Progressive renal failure (50 percent) ![]()

DIAGNOSIS of autosomal dominant policystic kidney disease

DIAGNOSIS family history; one or more of the symptoms mentioned. kidneys diffuse hyper-zoomed in on echogenicity and cysts on ultrasound. ![]()

Ultrasound and or radiological criteria for autosomic dominant policystic kidney disease

ULTRASOUND CRITERIA AND/OR RADIOLOGICAL (CT) 30 years: at least \< 2 cysts (mono-or bilaterally) [a sonographic finding negative does not exclude the pathology!] 30-60 years: at least 2 bilateral cysts 60 years \>: 4 or more bilaterally cyst [in order to minimize false positives due to renal cysts simple, frequent at this age]. Search for extra-renal manifestations in doubtful cases it!!! ![]()