glomerulonefritis skaidres Flashcards
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
Hystology of lupus nefritis
I -Normale
II - Mesangial GN
III - proliferative GN segmental and focal
IV - proliferative - diffuse GN
V - membraneous GN
Lupus nefritis clinic
Clinica
Segni extrarenali del L.E.S.
Urinary anomalies
S. S. Nefritica; S. Nefrosica
Lupus nefritis laboratory investgigations
less C3. ANA +, Ab>DNAs
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
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
ANCA-Positive vasculitis imunofluorescence
Negative; In some cases, deposits of Ig, C3 and fibrin
ANCA-Positive vasculitis clinica
Flu Syndrome, arthralgia, purple, asthma
and hemoptysis (sometimes)
Rapidly progressive GN;
variable proteinuria and hematuria;
arterial hypertension
Anca-positive laboratory exams
ANCA +: cANCA in GW;
pANCA in MPA. eosinofilin.
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
Functional alterations of diabetes
FUNCTIONAL ALTERATIONS
Glycosuria
Osmotic diuresis
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
Osmotic diuresis
Glucose is not reabsorbed increases urinary osmolarity reducing the reabsorption of water and sodium (mostly) resulting polyuria, polydipsia hypotonic edeplezioneidro-salina
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
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.)
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!!!
