e.g. against mesangial cells, endothelial cells or podocytes

injured cells produce substances (ROS, proteases, etc.) that damage the glomerulus

e.g. minimal change disease (see below)

activation of classic complement pathway → formation of membrane attach complexes (MAC) = "b-parts" → cell lysis

C3a + C5a → activation mastcells and release of reactive component (PG, Platelet activating factor, ROS, Lysosome enzymes, leukotriens)

C5a → attraction of Neutrophils and release of reactive component (PG, Platelet activating factor, ROS, Lysosome enzymes, leukotriens, IL, TNF) → activtion of Macrophages → more reactive substances and further cell damage

Thrombos → Microthrombi → ischemic events

Mesengial cells will produce reactive substances too (ROS, PG, Leukotriens)

Growth factor production by mesengial cells, macrophages and Lymphocytes → excessive proliferation of mesengial cells → compression of glomerular capillaries

1. Proteinuria >3,5g/24h
2. Hypoalbuminemia <3g (+/- hypoproteinemia <6g/dl)
3. Edema

normal serum albumin is 3,5 - 5,4 g/dl

↓ albumin → efflux water into interstitium → ↓ blood V → RAAS activation 📷

→Renin → activation Angiotensin → increased hydrostaic pressure

→ Aldosteron: Na + H2O retention

→ More fluid eflux out of vessels

→ hyperosmolarity (Na etc) of blood → triggers ADH → more H2O retention → more water efflux

edema is not caused by incr. hydrostatic capillary pressure but by low oncotic pressure → edema is not gravity dependend

👁️ peri-orbital (= loose tissue) → fluid efflux in the loose tissue doesn't ↑ the local pressure first → more fluid can accumulate

Periorbital (albumin-related edema doesn't follow gravity)

↓

Peripheral pitting

Pleural/Pericardial effusion + ascites

↓

Anasarca = generalized edema

• hyperlipidemia/dylipidema + xanthoma/xanthelasma, (+lipiduria arterioscleorsis+CAD risk)
• hypercoagulable state → increased risk of thrombosis
• Incr. susceptibility to infections
• Frothy urine (foam on beer 🍺)
• hypocalcemia + anemia→ in chronic stages
• symptoms of underlying diseases (e.g. malar rash in lupus)

F - Azotemia and hypertension are uncommon initially, but their presence may indicate advanced disease

Hematuria might also be present

see etiologies below

see etiologies below

artherosclerotic complication → MI, stroke

FSGS + membranous nephropathy

increased size (+/- number)→ non-selective proteinuria + hematuria

glomerular inflammation → GBM disruption

inflammated glomeruli swell up (inflammatory infiltrate, clots,..) → less blood flow to the kidney → decr. GFR

1. Hematuria with acanthocytes
‣
extrainfo
A type of dysmorphic red blood cell characterized by irregular, thorn-like cytoplasmic projections.

2. RBC casts
‣

extrainfos

RBC are stuck inside tubules 📷 → increase pressure from the fluid → get compressed with proteins

3. Hypertension → mild to moderate Edema + oliguria
4. Renal insufficiency (decr. GFR): esp. Azotemia + Crea (+ anemia)
5. Oliguria: inflammatory infiltrates reduce fluid movement across the membrane (↓ GFR) → oliguria + pyuria (leukocyturia)
6. mild - moderate Proteinuria <3,5g/24h

decreased GFR →less water excretion

→ activation RAAS due to less effective volume+Na reaching macula dense

→ Angiotensin → incr. BP

→ Aldosteron → water + sodium retention

GFR is reduced → you cant piss out se proteins

Possible development into Nephritic syndrome → Check for hematuria+ acanthocytes, RBC cast , Azotemia!

OR due to renal failure

attraction of macrophages + cytokines

stimulation epithelial cells → growth factor

⇒ extreme cellular proliferation in urinary space ⇒ cellular crescent ⇒ rapidly progressive GN ⇒ rapid renal failure + Uremia

post-streptococcal / post-infectious GN

IgA Nephropathy (Berger disease)

= Rapidly progressive GN

1. Goodpasture
2. Small vessel vasculitis
3. immune complex mediated diseases (like Lupus, IgA nephropathy, post-strep GN)

→ more details RPGN

Alport

• All causes for RPGN
• Lupus
• Alport

→ dont forget about Lupus which can manifest as diffuse proliferative GN

ACE-I or ARB

diuretics

Low sodium diet + water restrictrion

immunosuppression

plasmapheresis to remove antibodies

dialysis, transplantation

• child 4-8y
• heavy proteinuria + edema

normal

steroids

excellent herr specht wenn du treatest

ofc, makes 10-20% of adult nephrotic syndrome, but in the exam its gonna be child for sure ;)

reabsorbed lipoproteins → lipid accumulation

(hence the term "lipoid nephrosis" as a synonym of minimal change d.)

idiopathic / primary

NSAID, penicilliam, lithium

Hodkin's lymphoma → inc. cytokines

• allergy (sting 🐝 🦂 , vaccination)
• malignancies: lymphoma, leukemia, tumor

abnormal T-cells are activated due to previous infection (e.g. upper resp. trakt) → production of cytokines

→ damage of the footprocesses → effacement of the podocyte + structural changes of slit diaphragm

→ less polyanions (negative charges) are produced → albuminuria (negative charge + small) = selective proteinuria (bigger immunoglobulins can't pass)

• pure nephrotic syndrome (no nephritic sediment)
• Sudden onset selective proteinuria + renal edema
• normal renal function (GFR, Crea, Urea normal)

children 1-12 → MCD should be presumed if no other suspicion

• adults
• children with: concomitant nephritic syndrome, RF, steroid resistance (no response after 8 week)

Electronmicroscopy

(IF negative, light microscopy show nothing)

all normal/no findings

diffuse loss and effacement of foot processes

• non-specific treatment for nephrotic syndrome
• Corticosteroids
• Etiology if secondary

⇒ Immunsupressiva:

Cyclophosphamide → Eliminierung regulatorischer T-Zellen und Inhibition von T-Zell-Wachstumsfaktoren

or Cyclosporin → inhibits cytokine synthesis

Mycophenolat

wirkt als Inhibitor der Inosinmonophosphat-Dehydrogenase (IMPDH) und hemmt dadurch die Synthese von Guanosin.

B- und T-Lymphozyten sind in ihrem Wachstumsprozess aber auf eben diese Nukleotide (wie Guanosin) angewiesen. Dadurch sinkt deren Gehalt stark ab und eine effektive Immunreaktion ist unmöglich.

high mortality rate! → Infection + thromboembolism

>80%, 1-2 years

more than half!

• podocyte injury → scarring → proteinuria → progressive chronic kidney disease

• idiopathic - probably due to circulating permeability factors
• genetic - mutation in specific podocyte genes

• Viral infections (HIV, HepC, EBV, CMV)
• Drug-induced (Heroin, anabolic steroids)
• Adaptive due to:
• reflux nephropath, any advanced renal disease
• vascular abnormalities (hypertension, thrombus, stenosis, microangiopathies..)
• Obesity

IDIOPATHIC → prop. circulating permeability factors → podocyte lesion

dysfunction

detachment

foot process effacement

→ parietel cell cover GBM

→ synechia (cellular adhesion of Bowman's capsule with tuft)

→ hyalinosis 📷 + sclerosis

nope → some progressive bullshit

nephrotic syndrome

Biopsy

focal + segmental distribution of hyalinosis + sclerosis lesions (Terminology - what does focal segmental mean?)

could be igm + complent +

focal + granular pattern

diffuse effacement of footprocesses

patchy effacement

false negative → only biopsy of areas without abnormalities → >15 glomeruli!

non specific treatment of nephrotic syndrome

primary → generally good response to immunosupressive (esp. glucocorticoids) + RAAS

secondary → symptomatic + etiological treatment → ACEI/ARB (decr. glomerular pressure)

• ACEI / ARB
• sodium restriction

Predni

ACEI + ARB

Cyclosporin

mycophenolate, rituximab

depends in etiology

ACEI + ARB

statins

sodium restriction

underlying etiology

75% → very poor prognosis

50%

30% recurrence after (esp. primary idiopathic!)

→ give immunosupression!!

GBM thickening in response to igG + complement deposition

→ no cellular proliferation!

• Anti-PLA2R
• Anti-Thrombospondin (THSD7A)
• Anti-Neutral endopeptidase

MAID 👧

Malignancies (CA, Lymphoma, Leukemia)

Autoimmune (Lupus etc.)

Infections (HepC+B; HIV, siphilis, parasites)

Drugs/Toxins (NSAID, penicillamin, lithium, Captopril(ACEI)

linked to active disease + risk for renal failure

pretty certain

high specificity

75%

immunosupressive therapy might cause worsening if the etiology is an infection or cancer

cancer-associated MN has usually no tumor symptoms 🤓

Lung, prostate, digestive

PLA2R, THSD7A, neutral endopeptidase

• nephrotic syndrome presentation
• evtl. hematura + HT

normal at presentation → may develop into CKD

Anti-PLA2R

thickening GBM / capillary loops

no cellular proliferation, excudation or necrosis

(spike - dome pattern: subepithelial deposits seperated by BM projections → can be seen better in EM)

global, diffuse, granular (spincled) pattern of IgG + complement along subepithelial GBM; (epithelial side)

dense subepithelial immne complexes

spikes of lamina densa

→Later: Engulfed within GBM + thickening

"spike and dome pattern"

• CV-events → thrombolism, renal vein thrombosis, Pulmonary emoblism
• Chronic KD progression

albumin levels → low albumin = high risk

nonspecific + prophylactic anticoagulation

+/- immunosupression → depends on severity

Corticosteroids + cylclophosphamide

nonspecific NS:

ACEI or ARB

Statins

for 6 month

immunosupression

non-remitted after 6 month

severe symtpoms

progressive renal insufficiency

GFR<30 + evidence of sclerosis

• Ponticelli: monthly alternation steroids + cyclophosphamide
• other immune supressive
• Calcineurin inhibitors (cyclosporin)
• Rituximab
• Mycophenolate

nephrotoxicity!

B-cells

at least as effective in remission as ponticelli

very good → progressive renal insufficiency only 10%

GFR + Albuminuria

• severe chronic proteinuria
• reduced GFR → further declining

mainly nephritic

(nephrotic sydrome → rare)

Berger disease

very low

20% of all ESRD!

Pentru ca very high prevalence → most common primary GN

• The cause is still not entirely understood.
• Most likely mechanism: increased number of defective, circulating IgA antibodies are synthesized (often triggered by mucosal infections, i.e., upper respiratory tract and gastrointestinal infections) -> IgA antibodies form immune complexes that deposit in the kidney -> glomerulonephritis (typeIII hypersensitivity reaction)

• inflammations:
• Cirrhosis
• GI (inflammatory bowel)
• Psoriasis
• Immune (ankylosing spondylitis)
• infectious (HIV, Hep b+c)
• malignancies

• Incr. synthesis of abnormal IgA due to Glactose deficient IgA1)
• reduced clearance

→ aggregation + mesangial trapping

→ Anti-glycan antibodies against IgA → ICF in mesengium

→ Cytokines, mesangial proliferation → Complement activation

→ RIP

yes, has been demonstrated in at least some cases

occurs within 2 days of a febrile mucosal illness!

DD: Post-streptococcal GN → 10-20 days after infection(esp. tonsillitis)

• Assymptomatic → only change in laboratory parameters (e.g. microscopic hematuria+proteinuria→ can already have decr. renal function at presentation
• Reccurent episodes of:
• Macroscopic hematuria
• flank pain
• fever (usually low grade)
• Nephritic syndrome
• → esp. in relation to infection (GI + respir.)
• esp. in children
• Can progress to RPGN and/or nephrotic syn. (10% of patients)
• ARF with macroscopic hematuria
• 50% → develop ESRD within 20-25years

• Post-streptococcal → low C3,C4 10-20days post infections
• Lupus → low C3,C4, dsDNA, ANA
• MPGN

⇒ in IgA C3 usually normal because its not activated that extremly

Normal or MEST-C

• normal glomerulus
• Mesengial hypercellularity → assymptomatic
• Endocapillary hypercellularitý → acute GN
• Segmental glomerulosclerosis- chronic GN or ESRD
• Tubular atrophy + interstitial fibrosis
• Crescents → RPGN (crescent in 1/3 but only 5% have ≥50% crescent (to classify for RPGN))

mesengial diffuse global deposits of IgA 📷

→ Aim: reduce proteinuria, symptoms + complications

• ACEI/ARB for 3-6 month → ↓Proteinuria + ↓BP
• tonsillectomy if reccurrent
• (Statins → ↓cholesterol)

if RAAS-inhibit shows no improvement after 6month

• persistant proteinuria >1g/day after 6 month of ACEI
• Nephrotic syn + GFR >50
• Esp. budesonide

Immunsupressiva!

Predni for 3 days → then monthly i.v. cyclophosmaide for 6 month → maintenance treatment with azathiprine

Calcineurine inhibotrs (cyclosporin) + Rituximab

Renal replacement therapy / kidney transplantation in ESRD

Yes, but slow progression also nicht so schlimm lel

varies widely

1/3 → complete remission

1/3 → benign chronic persistant hematuria + proteinuria <1g/24h

1/3 → progressive decline in GFR → ESRD in 20years

HT

How bad is the proteinuria?

Inital renal function impairment

don't forget about the genetic IgA-NP

IgA in small vessels (capillary, venules, arterioles)

Skin (purpura)

Gut (abd. pain)

Kidney (GN)

Artralgia + arthritis

Same as IgA NP

in most cases symptomatic

→ renal manifestations same as IgA NP

biopsy

skin, joints, MSK, heart, lungs, NS, any other..

SLICC classification 📷 [Systemic lupus international collaborating clinics]

• 4 out of 17
• at least one out of each group

biopsy + ANA or dsDNA pos.

80%

jap

• complement activation
• leucocytes infiltration, cytokines, procoagulant factors

= infiltration + proliferation → inflammatory glomerular disease

Glomerular injury, but no inflammation 🤡

any of..

• persistent proteinuria (>3+ dipstick, >0,5g/day)
• active urinary sediment (RBC cast)

• Hypocomplementemia
• ANA, anti-dsDNA, Anti-Sm

biopsy

Antiphospholipid syndrome 📷 → Thrombotic prhoylaxis

nonspecific - ACEI, ARB

if nephrotic syndrome → corticosteoroid or calcineurin inhib(cyclosporin)

• nonspecific
• Immunosuppressive:
• induction: corticosteroids + cyclophosmadie or mycofenolat mofetil (MMF)
• maintenance: corticosteroids + azathiprine or MMF

corticosteroids + immunosuppressive (cyclophosphamide, cyclosporin, MMF, azath) for 1-2 years

no immunosupression!

renal replacement in ESRD, transplantation when no sign of activity

• Hydroxyclorochine in any class (against onset, relapses, ESRD)
• NSAID in skin/joint involvement
• Plasmapheresis in RPRF-associated LN, anitphosphlipidic syndrome, hemolytic-uremic syndrome

like initial regimen

→ if resistance: Rituximab, etc.

high crea

HT

Nephrotic range proteinura

Anemia

Black, hispanic

Class IV, crescents + associated tubulinterstital

ANA, Anti-dsDNA, C3, C4, Proteinuria, urinary sediment, Crea, eGFR, biopsy

• acute nephritic syndrome →Acantocytes+RBC-casts, non-nephritic proteinuria
• glomeruloar crescent formation with progression to renal failure within weeks to month ⇒ ACUTE RENAL FAILURE

≥2 layers of proliferating cells in Bowman's space

• proliferation of epitelial cells (parietal)
• Mp

= cellular crescent

• fibrinoid necrosis of the capillaries

= fibro-cellular crescent

Types:

1. Anti-GBM-mediated: Goodpasture

→ igG linear pattern along GBM

‣
IF picture

2. Immune complex mediated: Lupus, IgA nephropathy, post-strep GN [LAP]

→ granular complement deposition in capillary wall 📷

3. Pauci-Immune:

systemic small vessel vasculitides including: microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (EGPA), and granulomatosis with polyangiitis (GPA)

→negative/little immunofluorescence pattern

in all types → crescent formation 📷

• poor prognosis (if untreated)
• Tx:
• Anticoagulation
• Plasmapheresis + Immunosuppressants
• Dialysis
• Transplant

• poor prognosis
• behaves like Anti-GBM ealry
• relapses like ANCA-vasculitis

ß-pleated sheet fibrillar proteins

proteases can only cleave alpha-structured proteins

→ ß-pleated proteins can't be removed → insoluble

→ accumulation → locally or widely(multiorgan failure)

from mild albumiuria - nephrotic syndrome

• chronic inflammation (AA) → incr. no. of Serum amyloid A (SAA)

• multiple myeloma (AL)→Abnormal plasma-cells → abnormal proteins → amyloidosis
• hereditary: esp. fibrinogen A-alpha mutation

alzheimer

congo red

amyloid P component

non-branching fibrils 📷

rare shit

yes in risk group:

cause for 17% of nephrotic syndrome in patients over 65y

MONOCLONAL GAMMOPATHY (esp. du to multiple myeloma 20%)

⇒ Free light chains (esp. Lambda, kappa)

GBM + Mesengium

become thick

→ tissue toxicity

multiple myeloma -syndrome

peri-orbital brusing (due to thrombocytopenia?)

macroglossia

edema

nephrotic syndrome

cardiac dysfunction

nerve abnormalities

• serum free light chain test - detects 98%
• Serum + urine proteins electophoresis

Serum amyloid P scintigraphy 📷

BIOPSY of:

bonemarrow, kidney, liver, fat, fums,..

ye, 80%

proteins - variable range

mild albuminuria - nephrotic syndrome

bland sediment

Bence-Jones proteins

• Fanconi Syndrome due to Bence-Jones proteins which obstruct the tubular lumen → NaK-pump insufficiency → resorption impared

⇒ renal tubular acidosis

ne nicht wirklich

• Amyloid in all structures 📷
• thick GBM, expanded Mesangium
• Eosinophil nodules
• Late: Sclerosis

Congo red: 📷

Green birefringence in Congo red with polarized light: 📷

• neg. for Ig + complement
• positive for lambda or kappa (not both simultaneously)

non-branching amyloid fibrils 📷

• classic nephrotic nonspecific (RAAS,diuretics)
• myeloma specific → chemo, stem cell transpl.
• RRT/transplant

• if myeloma → myeloma protocol (chemotherapy)

→ Election therapy: CyBorD

• Symptomatic (diuretics, Anti-Proteinuric agents(ACEI/ARB), dialysis)
• stem cell transplantation
• kidney transplantation

• cardiac (arrhythmias, blocks, failure)
• ESRD
• extra-renal manifestations:

“DER FETTE KRIECHENDE TUNNEL MENSCH”

1. neuropathy
2. carpal tunnel
3. hepatomegaly
4. macroglosia
5. pulmonary infiltrations
6. clotting abnormalty

only 30%

nephritic

• poststrep-GN
• infective endocarditis -relatedGN
• shunt nephritis

rare

children 6-10y

Strep + Staph

HIV, Hep B+C

acute 10-20d

• Upper resp. tract infection, GAS (pyogenes)
• 1-4 weeks ago (DD: IgA NP - days after)

Blood:

• ↑ Anti-SLO
• ↓ C3

Endothelial + Mesangial cells → diffuse proliferation + Np infiltration

"STARRY SKY" 📷

• in Mesangium + Capillary walls → diffuse granular IgG, IgM + C3

Subepithelial humps 📷

supportive/symptomatic treatment

• sodium + fluid restriction
• Loop diuretics (esp. when edema)

• when other treatment doesn't correct the fluid overload
• Uremia → might develop uremic encephalopathy

corticosteroids (methylpredni)

Only in chronic, recurrent infections

Antibiotics , Antimicrobials

Alles entspannt, usually resolves within 6 weeks

Fluid overload leads to:

• Hypertensive encephalopathy
• Heart failure
• Pulmonary edema

nephritic syndrome lead to:

• ARF

• HbA1c ≥6,5 or
• fasting Glu >126 or
• Glu ≥200 at any time

• leads to sclerosis + fibrosis
• progressive albuminuria

→ HT + renal insuff

• other GN
• Neurogenic bladder (neuropathy) → obstruction
• UTI
• Vascular nephropathies
• Papillary necrosis

nephrotic

type 2 → 90%

hell yea, the most common

• genetic
• poor glycemic control
• HT
• Proteinuria
• low GFR
• Incr. Proteinintake
• metabolic syndrome (hyperlipid, obesity, smoking)

Chronic hyperglycemia → non-enzymatic glycosylation (NEG) of the basement membrane (protein glycation) → increased permeability and thickening of the basement membrane and stiffening of the efferent arteriole → hyperfiltration (increase in GFR) → increase in intraglomerular pressure → progressive glomerular hypertrophy, increase in renal size, and glomerular scarring (glomerulosclerosis), GBM thickening, mesangial matrix expensian, podocyte injury → worsening of filtration capacity

keine! 🤡praaaaank

• proteinuria esp. macroscopic/severely inc. albuminuria >300mg / 24h
• Renal edema
• HT
• RF → ESRD with uremic syndrome

microalbuminuria

30-300mg/24h

diabetes: crea + proteine increase at the same time.

if not increase at the same time ⇒ unlikely to be diabetes

albuminuria/24h ⇒ 30-300g/24h

albumin/crea ratio ⇒ 30-300mg/g

only when blood sugar levels are high

→ not related to diabetic nephropathy

nope, only levels over 300mg/day, → urinary exame might be normal, despite microalbuminuria

every year

albuminuria → albumin/crea ratio (when there is no infection present)

→ abnormal test ⇒ again in 3-6 month

• exercise
• fever
• UTI
• HT

→ if presentation with hematuria!

type 1 → 90%

type 2 → 60%

that it might NOT be diabetic nephropathy

• severely incr. albumin + bland urinary sediment OR
• moderatly increased albuminuria + retinopathy

noooo

• proteinuria in less than 5 years after DM-1 diagnosis
• no retinopathy in DM-1
• active urinary sediment (nephritic)
• ACUTE onset of RF/nephrotic sy → albumin >3,5g/24h (crea usually normal)
• clinic of another systemic disease

normal / incr. size

normal echogenicity of parenchyma (even in ESRD)

Class I: GBM thickening

Class II: Mesangial expansion

Class III: Kimmelstiel-Wilson=nodular intercapillary glomerulosclerosis (<50% of one glomerulus)

Class IV: Advanced sclerosis

glomerulosclerosis starts diffuse and than becomes nodular

Hyaline thickening of efferent and afferent arteriole → narrowing + vasdilation of afferent

⇒ Interglomerular hypertension

negativ OR non-specific linear IgG (low intensity)

• thickend GBM
• Mesanagial expansion

nephortic + chronic + diabetic specific management

• lifestyle → keine faules, fettes, ungesundes, rauchendes schwein mehr
• hyperglycemic control
• ACEI, Arb, Diuretics
• statins
• Low protein diet (0.8 g/kg/day)
• Treatment of anemia + hPTH
• planning RRT

• adjustment to GFR
• Metformin lactic acidosis in decr. GFR (better switch to insulin)

nope

10-12 ml/min/year

albuminuria severity

annual risk:

• No nephropathy - 1% risk of death; 2% risk to progress;
• Microalbuminuria-3% risk of death; 2,8% risk to progress; Macroalbuminuria - 5% risk of death; 2,3% risk to progress;
• ESRD- 19% risk of death.

arm wie n schwein

immune-mediated infammation → infiltrate in kidney intersititium → ARF

15%

1. Drugs 75% - not necessarily nephrotox but hypersensitivity reaction
2. Autoimmune (SLE, Sjögren syn)
3. Systemic Infections (CMV,EBV,Legionella,Strep)
4. TIN with uveitis syndrome (TINU syndrome) 📷
‣

💬

TINU syndrome • TINU (Tubulolnterstitial Nephritis + Uveitis) • First described in 1975, by Dobrin • More than 150 cases were reported Pathogenesis • Unknown • Renal tubular & ciliary body epithelia: electrolyte transporters sensitive to carbonic anhydrase inhibitors -> share common autoantibody? • Cell-mediated immunity, delayed-type hypersensitivity?

Risk factors No identifiable risk factors have been found • Infection (Chlamydia, EBV), drugs (antibiotics, NSAIDs), "goreisan," • Autoimmune diseases (hypoparathyroidism, hyperthyroidism, IgG4-related autoimmune disease, RA)

• AB → Penicillin, Cephalosporins
• NSAID
• Diuretics

1. Hypersensitivity reaction to drug
• Drug mimic nephritogenic AG
• Drugs are trapped in interstitium

⇒ Ag-Ab-complex → immuneresponse + infiltrate → tubular injury

2. Acute cellular injury caused by infection (often associated with obstruction or reflux)

• Rash
• Fever
• Eosinophilia

in acute kidney injury

Big variation in clinical picture: asymptomatic - RF

• Microhematuria,
• Eosinophilia (Hypersensitivity),
• Leukocytecast +Leukocyturia,
• mild proteinuria = Tubular proteinuria <1,5g/24h

• Glycosuria
• Phophaturia
• Aminoaciduria

Na/k-P:

→ Hyperkalemia

→sodium wasting

→ Acidosis (distal tubular)

Aquaporin:

→ nephrogenic diabetes insipidus

when diagnosis is not clear

→ definite dg by biopsy

highly suggestive!

T-Lym, Mp, Mc, Eos, Np

→ interstitium → edema

→ tubular BM→ Tubulointerstitial nephritis → necrosis tubular cells (!!epithelial cells + casts still indicate Ac. tubular necrosis ATN)

Drug withdrawal

→ kidney bioposy + glucocorticoids

Antimicrobial treatment

RRT → hemodialysis

and other supportative treatment

Just easy money drug withdrawl

• inflammation tubules + interstitium
• slow progressive chronic renal failure (month-years)

Etiology → Renal cell injury → Expression new local antigens → inflammatory infiltrate, cytokines in interstitium + tubules

• Leukocyturia, w/o bacteriuria, mild proteinuria → bland sediment
• Fanconi sy: Proximal tubular dysfunction + glycosuria, amnoaciduria, phosphatura, proximal renal tubular acidosis)
• HT
• slow progression to ESRD
• Assymetric renal involvement → obstruction, reflux only affect one kidney
• small, atropic kidney

• etiology + supportative
• AB in reflux + obstructrion
• surgical intervention

• outside hospital aquired + hospital aquired
• sensible germs + resistance germs

bacteriuria + leucocyturo

→ repeat exam!

could be do to contamination of sample or contamination via catheter

• atypical germs
• other inflammatory causes → stone, tumor, irradiation damage, nephrologic D

G- → E.coli, Klebsiella, Enterobacter, Proteus

G+ →Enterococc(Klebs, Pseudomonas), StaphAureus

*most common - assiciated with infection outside hospital, others are nosocomial

• Neisseria gonorrhea
• clamydia
• staph + strep

cloudy 📷, bad smell

+/- hematuria

dipstick (leukoC-esterase, nitrite)

1. Vesicoureteral reflux
2. Obstruction: Disruption urinary flow
1. foreign body (catheter, ureteral stent, nephrostomy)
3. NM: neurologic bladder + sphincter abnormality
4. female RF
1. postmenopausal
2. pregnancy

→ When SEPSIS → check for obstruction/Abcess → treat immediately

CT: can detect: gas-forming abcess, hemorrhage, obstruction, anatomic factors

• reflux
• obstruction
• pregnancy
• pre-urologic procedure
• neutropenia
• recent transplant

acute pyelonephritis in 25-40%!

→premature delivery, low birth weigh, baby mortality

! SCREEEEEEENING bidde

Amoxi-Clavu or Phosphomycin

no Fluros, no TMP in first trimester

all have bacteriuria → absent/minimal symptoms

Remove catheter, do intermittent cathetering, only treat when symptomatic (fever,dysuria)

• Forunier gangrene

• Procalcitonin → incr. in big amount of bacterial, fungal + parasitis

• AB asap!

→ start empiricial broad spectrum early → then adapt to antibiogram

• give volume
• vasopressor (NE,dobutamin)
• evtl. cortisone in renal failure

crystalline mineral deposits → migrate + obstruct UT → renal colic pain

Classic: Colic wave pain+ Hematuria

severe: UREMIC SYNDROME + SEPSIS

= site of pain

• Diet
• reduced water intake
• HT
• DM
• disorders leading to high Ca

• calcium oxalate - most common 75%
• calcium phosphate - 15%
• uric acid - 10%
• struvite, cystein - rare

• hypercalciuria + oxalaluria due to any cause (hPTH)
• obstruction of the ureter or UPJ
• animal protein intake, vitC + D intake

Proteus + Klebsiella (Urease-producing) → only in upper UTI

• Ions (Ca, P)
• Urea + Crea
• Uric acid
• PTH
• CRP, WBC
• Hb, Hct

• Dipstick - Hematuria
• Infection (Leu, nitrate,ph,culture)

US → Hydronephrosis? Stone?

→ CT (without contrast) → Confirm diagosi(stone/hydronephrosis)

KUB → radioopague; in uric acid → detection with IVP

with contrast: Retrograde pyelography or UroCT → if stone removal is planned

PAIN + DECOMPRESSION + AB

• Pain control → NSAID, Opiates, warming,
• MET: alpha-blocker + ca-channel blocker 📷
• UTI + Sepsis → AB
• Prevention + Recurrance
• Diet →VitC, animal prot, Na, Ca, purine in uric acid
• sufficient Fluid intake → 2.5-3L/day
• sodium restriction if high excretion
• Drugs → thiazide (↓urinary Ca elimination)
• Lifestyle advide → normal BMI
• treat Hyperparathyroidsm
• Urologic intervention

1. Chronic • Hypertensive nephrosclerosis • Renal artery sclerosis and ischemic nephropathy •Antiphospholipidic syndrome •Cholesterol crystals emoli
2. Acute/ Rapidly progressive •Acute hypertensive nephrosclerosis •Thrombotic microangiopathies •Sclerodermic renal crisis

• Chronic essential hypertension (HT)
• Proteinuria (<1-1.5g/day)
• Progressive renal insufficiency (slowly progressive)

up to 30%

→ 12- 30% of patients with dialyzed patients with ESRD are caused by hypertensive nephrosclerosis

• HT present BEFORE renal involvement
• sign secondary to HT:
• Hypertensive retinopathy
• Left ventricular hypertrophy
• no other cause of renal diseases
• progressive renal damage (crea +urea)

• prexisting CKD
• HT
• black race

• Relatively normal urine sediment (+/- microscopic hematuria)
• Proteinuria <1-1,5 g/24 hours
• Ultrasound: Symmetrical small kidneys

nope,not indicated

• Treat hypertension
• Decrease cardiovascular risk
• Slow the progression of CKD
• Treat the complications of CKD

• lifestyle change (low salt+protein, sport)
• treat aggravating factors
• infection
• avoid toxins, drugs, dehydration
• BP control
• ACEI, ARB if proteinuria
• calcium channel blocker, loop diuretics, betablockers

if crea rise more than 30% → suspect bilateral arterial stenosis📷

⇒ otherwise continue

slow progression to ESRD

→ other complications associated with HT (also malignant hypertension → acute hypetensive nephrosclerosis

• malignant hypertension due to stop of antihypertensive drugs → BP >180/120
• RF, Hematuria, high proteinuria
• HT-ecephalopathy, Cardiac failure, retinal hemorrhage

Hell no

fibrinoid necrosis 📷 → only in bloodvessel

• normal protein
• different sizes of right + left kidney
• hypertension

Patholo (see below) → reduction of renal artery lumen → decrease perfusion of kidney → RAAS activation → intrarenal ischemia

• renovascular hypertension
• ischemic nephropathy

bilateral (or unilateral stenosis and single kindey that works)

• Age at onset of HT below 30 or above 55
• Acute HT
• Abrupt onset of HTN or acceleration of previously stable/ well controlled BP
• Severe/refractory hypertension to an appropriate 3 drugs regimen
• Malignant HTN
• Recurrent "flush pulmonary edema"
• Acute renal failure after RAAS inhibition treatment (creatinine rise >50% baseline value within 1 week after ACE/ARBS treatment)
• Moderate/severe hypertension in a patient with generalized atherosclerosis/ or asymmetry in renal size >1.5cm
• Systolic-diastolic abdominal bruit (sensitivity 40%, specificity 99%)

• clinical
• Doppler, angio MRI/CT
• contrast angiography 📷 - gold standard, but invasive

⇒ how severe is the stenosis? → treatment

contrast medium: further deterioration of renal function / allergy

Renal arteriography - gold standard

• confirmation of diagnosis and cause of renal artery stenosis (if >75% stenosis + clinical context => indication for intervention)
• extent of intrarenal vascular disease

• ACEI + ARB
• diuretic

⇒ if crea > 30% stop ACEI,ARB!

• bilateral high grade ( > 75%) arterial stenosis/ or unilateral in solitary kidney
• uncontrolled HT with optimal treatment (3-5 drugs)
• progressive decline in GF/ rapid raise in serum creatinine during HT treatment
• severe decrease in GFR after ACEI/ARBs therapy
• recurrent congestive heart failure => repeated "flush pulmonary edema"
• kidney size >9 cm
• before advance kidney failure (creatinine more>3-4mg/di indicates irreversible lesions)

75-90%