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Medical Internal Medicine-UrologyDiseases
This is a mind map about medical internal medicine-urinary system diseases, including rapidly progressive nephritis, Nephrotic syndrome, primary glomerular disease, etc.
Edited at 2023-11-28 17:00:05- bacteria
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Medical Internal Medicine-UrologyDiseases
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- Outline
urinary system
urinary tract infection
Overview of urinary sensation
Ascending/retrograde sex is more common, more common in women
E. coli is more common (especially uncomplicated, first-time occurrence, asymptomatic)
Proteus
With urinary tract stones
Staphylococcus aureus
Hematogenous urinary sensation
Pseudomonas aeruginosa
After urinary tract instrumentation
complex urinary sensation
With urinary tract structural or functional abnormalities
Immunocompromised (kidney transplant, etc.)
Occurs on the basis of chronic renal parenchymal disease
asymptomatic bacteriuria
No clinical symptoms, but two urine cultures were positive for the same species
Short course of treatment: pregnancy, children, complicated urinary syndrome, symptomatic infection
Auxiliary inspection
Nitrate reduction test (screening)
G-bacteria positive (high specificity)
Urine routine
Almost pyuria (WBC>5/HP)
Some have hematuria (RBC>3/HP) and proteinuria (>0.15g/d)
True bacteriuria/urine culture (gold standard for acute urinary tract infection)
≥100,000/ml
Intravenous pelvis/urography IPV/IVU (gold standard for chronic pyelonephritis)
Unilateral or bilateral asymmetric narrowing, renal pelvis and calyces deformation
Pyelonephritis is more common:
White blood cell casts, urine NAG↑, urine β2-MG↑ (β2-microglobulin), positive urine culture after bladder flushing, urine specific gravity and osmotic pressure↓ (common in chronic cases)
Clinical manifestations and treatment: (all may have urethral irritation)
acute cystitis
Obvious pyuria, no systemic symptoms
treat
Young non-pregnant women: 3 days
Others with low resistance: 3-7 days
First-line drugs: cotrimoxazole (sulfamethoxazole and trimethoprim), nitrofurantoin, fosfomycin
acute pyelonephritis
Some patients do not have signs of urethral irritation
Obvious pyuria, white blood cell casts, systemic symptoms (T＞38℃, blood WBC↑), and percussion pain in the kidney area
If the body temperature rises again, severe low back pain and colic → complicated by renal papillary necrosis (sepsis, infectious toxic shock, pyonephrosis, perirenal abscess)
treat
2 weeks
Relapse (same pathogen as last time): 6 weeks
More than 2 attacks within half a year: 6 months (long-term low-dose bacteriostasis)
chronic pyelonephritis
Chronic disease course, IPV renal calyceal pelvic deformation, persistent tubular condensation and other functional impairments (urine specific gravity and osmotic pressure ↓)
There may be decreased glomerular filtration (blood Cr↑, BUN↑) and secretory function (renal tubular acidosis, PSP↓)
urethral syndrome
No systemic symptoms and no true bacteriuria (mycoplasma infection probably)
kidney failure
acute kidney injury
Pathogenesis
Prerenal (most common)
Effective circulating blood volume↓
Capillary blood pressure↓
Renal (ATN, interstitial nephritis, etc.)
Renal ischemia, renal poisoning, original urine leakage, renal tubular obstruction
Postrenal
Urinary tract obstruction
Renal intracystic pressure↑
Prerenal AKI vs ATN
Staging and treatment
installment
Starting period
Oliguric phase (progression/maintenance phase)
High potassium, high magnesium, high phosphorus, low calcium, low sodium, low chloride, water intoxication, metabolic acidosis
Main causes of death: hyperkalemia, water intoxication
Polyuria period (recovery period)
GFR can return to normal first (rich blood flow), and other indicators can return to normal later.
Main causes of death: hypokalemia, infection
When correcting acid, be careful to prevent tetany of the hands and feet caused by reduced free calcium (hypocalcic twitching)
chronic renal failure
toxin
small molecule toxins
K, P, H, urea nitrogen, amines, phenols. Can cause impaired glucose tolerance
medium molecular toxin
Parathyroid hormone PTH (can cause renal osteodystrophy, soft tissue calcification)
Macromolecular toxins (proteins)
Ribonuclease, lysozyme, β2-microglobulin, vitA binding protein, carbamylated protein
clinical manifestations
digestive system
appeared first
Digitalis poisoning first appears as digestive system symptoms
circulatory system
Main cause of death: heart failure
Sodium and water retention, hypertension, cardiomyopathy, pericarditis, anemia, electrolyte imbalance and acidosis
blood system
Mild to moderate anemia (EPO↓) and bleeding (reduced platelet function) are common
vs: AKI usually has mild anemia (severe course)
Give EPO, iron, folic acid
osteodystrophy
high transformation bone disease
Excessive PTH, fibrocystic osteitis, easy fractures
Renal failure → calcitriol ↓ → low calcium → too high PTH (secondary hyperparathyroidism) → osteolysis
X-ray skeletal cystoid defects and osteoporosis
low conversion bone disease
osteomalacia
Calcitriol deficiency, aluminum poisoning
bone dysplasia
PTH is relatively low and osteogenic factors are insufficient
mixed bone disease
installment
Blood Cr>265 should not use ACEI/ARB
treat
Control urinary protein and high blood pressure: ACEI/ARB
Blood pressure <130/80
If urine albumin/creatinine <30 or dialysis, blood pressure <140/90
Water restriction, sodium restriction, phosphorus restriction (using phosphorus binders: sevelamer, lanthanum carbonate), protein restriction, lipid restriction, drug restriction (aminoglycosides, first and second generation cephalosporins, traditional Chinese medicine containing aristolochic acid)
dialysis
Indications
K>6.5
ph<7.2
cr>442 (acute)/707 (chronic)
BUN＞21.4
Exacerbation of uremia (pericarditis or severe encephalopathic epilepsy)
Severe pulmonary edema refractory to diuretics
method
intermittent hemodialysis
Continuous renal replacement therapy CRRT: continuous veno-venous and arterio-venous hemofiltration
peritoneal dialysis
related complications
high output heart failure
Dialysis-associated pericarditis
aggravate atherosclerosis
Unable to correct lipid metabolism disorders
bone dysplasia
dialysis imbalance syndrome
Dialysis-related amyloidosis of bone
Primary glomerular diseases (overview)
Overview
Classification of glomerular diseases
primary
It starts in the glomerulus, or the cause is unknown. More common in men
Secondary
Systemic disease causes glomerular damage. Such as diabetic nephropathy, lupus nephritis, microscopic polyangiitis
hereditary
Alport syndrome
proliferative inflammation
Gold standard: renal biopsy
Pathogenesis
Cellular immunity (T cell mediated)
minimal change nephritis
Humoral immunity
in situ immune complex type
Anti-basement membrane GBM
Rapidly progressive nephritis type I
Pulmonary hemorrhage nephritis Goodpasture syndrome (alveolar wall necrosis, hemorrhage, alveolar septal widening, fibroplasia)
Secondary rapidly progressive nephritis type I
antipodal membrane
Membranous nephropathy, Heymann nephropathy
Acute nephritis, rapidly progressive nephritis type II
circulating immune complex type
Acute nephritis, rapidly progressive nephritis type II
(SLE and Henoch-Schonlein purpura can lead to secondary rapidly progressive nephritis type II)
Mesangial capillary nephritis type I
Autoantibodies ANCA
Rapidly progressive nephritis type III
Microscopic polyangiitis, Wegener's granulomatosis
Secondary rapidly progressive nephritis type II
clinical manifestations
acute nephritic syndrome
Mainly seen in
acute nephritis
Rapidly progressive nephritis (rapidly progressive nephritic syndrome)
acute attack of chronic nephritis
concept
Hematuria (>3/HP): essential condition
Proteinuria (>0.15g/d)
Edema
Glomerular filtration rate ↓ leads to water and sodium retention, and edema starts from the eyelids and face
volume-dependent hypertension
There may be transient or obvious renal insufficiency
Urine output ↓, blood Cr (>100) and BUN (>8) ↑, anemia
chronic nephritic syndrome
Mainly seen in
chronic nephritis
concept
Hematuria, proteinuria, edema, and hypertension that persist for >3 months
Polyuria, nocturia, low specific gravity urine
Residual nephron overload
nephrotic syndrome
Mainly seen in
Lipoid nephropathy, membranous nephropathy, mesangial proliferative nephritis, mesangial capillary nephritis, focal segmental glomerulosclerosis
The difference between inflammation and disease is that "inflammation" involves the mesangial area (→ Damage to the basement membrane → Hematuria)
concept
Massive proteinuria (required)
＞3.5g/d
Hypoalbuminemia (required)
Albumin＜30g/L
Hepatic compensation increases albumin synthesis < protein loss
Marked edema
Plasma gel osmotic pressure↓
Hyperlipidemia
Mainly related to reduced decomposition
Asymptomatic hematuria and/or proteinuria (occult nephritis)
No edema, hypertension, or renal impairment
Regular follow-up without glucocorticoids and cyclophosphamide
acute nephritis
name
acute diffuse proliferative nephritis
postinfectious nephritis
Closely related to β-hemolytic streptococcus infection → There is a history of prodromal infection 1-3 weeks before the onset of illness (history of upper respiratory tract infection such as fever, sore throat, or skin infection, etc.)
Anti "O"
intracapillary proliferative nephritis
Endothelial cell and mesangial cell proliferation
Hump-like changes after deposition of immune complexes
pathology
Increased kidney size, large red kidneys, and flea bites on the kidneys
Granular fluorescence, hump-shaped electron dense matter
clinical manifestations
Indications for kidney biopsy
With worsening kidney function
Oliguria for more than 1 week or progressive decrease in urine output and continued increase in serum creatinine
with nephrotic syndrome
The disease lasts for more than 8 weeks and there is no improvement trend
Treatment (mainly supportive of symptomatic treatment)
Use diuretics first, then ACEI/ARB or CCB
When acute nephritis attacks, most of the infection foci have been controlled.
Asymptomatic infection does not require antibiotics, otherwise penicillin is used
Recurrent tonsillitis can be removed after the condition stabilizes
No glucocorticoids or cyclophosphamide
Rapidly progressive nephritis
name
Extracapillary proliferative nephritis
glomerular parietal epithelial cell proliferation
crescentic nephritis
The basement membrane is obviously broken (basis of the lesion → massive exudation of cellulose)
Great White Kidney
rapidly progressive nephritis
The most prominent manifestation is the rapid deterioration of early renal function
Serum creatinine >200, almost >400
Have anemia
type
Type I - anti-glomerular basement membrane antibody type
In situ immune complexes, linear fluorescence
Lipid nephropathy, type III rapidly progressive nephritis: no fluorescence; Type I rapidly progressive nephritis: linear fluorescence
Secondary to Goodpasture syndrome
Type II-immune complex type
In situ - circulating immune complexes, granular fluorescence, electron dense matter, endothelial and mesangial cell proliferation, sustained complement C3↓
Secondary causes include SLE, Henoch-Schonlein purpura, and acute nephritis
Type III - Immune complex deficiency
ANCA, no fluorescence
Secondary diseases include microscopic polyangiitis (p-ANCA) and Wegener's granulomatosis (c-ANCA).
treat
Prednisone Cyclophosphamide
intensive therapy
Methylprednisolone impact enhancement
Type II, Type III
Intensive plasma exchange
Pulmonary hemorrhage (such as Goodpasture syndrome), type I, type III
Indications for dialysis
Kidney transplant
It needs to be done after the disease has stopped for half a year
nephrotic syndrome
complication
Thrombosis and embolism
Most common in membranous nephropathy
Renal veins most commonly involved
Sudden low back pain, worsening of hematuria and proteinuria, decreased renal function, and enlarged kidneys
Albumin＜20g/L
Prophylactic anticoagulation (heparin or warfarin), supplemented with antiplatelet (aspirin or dipyridamole)
Thrombosis and embolism have occurred
Anticoagulation, antiplatelet, thrombolysis (urokinase or streptokinase)
Protein and fat metabolism disorders (not water and electrolyte disorders)
Infect
Acute kidney injury (rare) (not renal failure)
Most common in lipid nephropathy
treat
Glucocorticoids (adequate initial dose, slow taper, long-term maintenance)
Starting: Prednisone 1mg/kg daily, 8-12 weeks
immunosuppressant
Commonly used cyclophosphamide (cytotoxic drug)
Hormone nephrotic syndrome refractory to cyclophosphamide: cyclosporine, mycophenolate mofetil
Different nephrotic syndromes respond to hormones to varying degrees
Lipid nephropathy, focal segmental glomerulosclerosis, and mesangial proliferative nephritis should be treated with steroids alone
Initial treatment of membranous nephropathy, mesangiocapillary nephritis and retreatment of all types: steroids cyclophosphamide
primary nephrotic syndrome
Lipid nephropathy
Special: only the charge barrier is damaged; T cell-mediated cellular immunity (the remainder is humoral immunity (in situ, circulating, ANCA)); Almost no hematuria
name
Lipid nephropathy
proximal tubule fatty degeneration
Podiatry
The foot process fusion of the epithelial cells (podocytes) in the visceral layer of the renal capsule disappears.
minimal change nephropathy
More common in children and adolescents
There are no obvious glomerular lesions under light microscopy (only the charge barrier is damaged)
classic nephrotic syndrome
Massive proteinuria, hypoalbuminemia, edema, hyperlipidemia
Almost no hematuria or hypertension
But kidney damage is common after age 60
Membranous nephropathy (common in middle-aged and elderly people)
The basement membrane is obviously thickened, with spike-like protrusions, moth-eaten spaces, and tooth-comb-like appearance.
There may be visceral podocyte foot process fusion
Lipoid nephropathy, membranous nephropathy (anti-foot process membrane), and focal segmental glomerulosclerosis can all have podocyte foot process fusion.
Mesangial proliferative nephritis (adolescents)
Mesangial cell and stromal proliferation
nephrotic syndrome
Almost all have hematuria
Mesangial capillary nephritis
membranoproliferative nephritis
Proliferation of mesangial cells and matrix, interposed between basement membrane and endothelial cells
Stratification sign, double track sign
type
Type I: Circulating immune complex type
Type II/dense deposit disease
Abnormal activation of the alternative complement pathway→C3 persistence↓
massive dense material deposits
nephrotic syndrome
almost hematuria
focal segmental glomerulosclerosis
secondary nephrotic syndrome
allergic purpura
Symmetrical purpura of both lower limbs
Mainly IgA deposition
SLE
More common in women of childbearing age
Hepatitis B
Membranous nephropathy is the most common
More common in children and adolescents
diabetes
bone marrow disease
Lymphoma
amyloidosis
More common in middle-aged and elderly people
IgA nephropathy
The most common glomerular disease in my country; the most common cause of glomerular hematuria
It can manifest into various pathological types: mesangial proliferative nephritis is the most common, and mesangial area IgA deposition is the most characteristic.
Prodromal infection 1-3 days before onset of illness
30%-50% of patients have elevated blood IgA (but not completely related to disease severity)
Treatment according to different types and manifestations
Simple microscopic hematuria (major)
Support symptomatic treatment and regular review of hematuria
Recurrent gross hematuria
Penicillin aggressively controls infection; chronic tonsillitis should be removed
With proteinuria and/or hypertension
ACEI/ARB control proteinuria to <0.5g/d.
If proteinuria still persists >1g/d after 3-6 months, prednisone can be given
with nephrotic syndrome
Mainly glucocorticoids
with renal failure
Differential diagnosis
Chronic glomerulonephritis (chronic/end-stage/sclerosing nephritis)
pathology
Massive glomerular fibrosis, glomerular concentration, and infiltration of lymphocytes and plasma cells
secondary hypertension
hyaline degeneration of small arteries
Secondary granular pyknotic kidney (symmetrical)
clinical manifestations
Slow onset and insidious onset
Chronic nephritic syndrome (>3 months), acute attack (acute nephritic syndrome)
B-ultrasound showed that the size of both kidneys was normal in the early stage and symmetrically reduced in the late stage (long diameter <10cm).
Treatment: The main goal is to delay the deterioration of renal function and prevent cardiovascular and cerebrovascular complications, not to eliminate nephritic syndrome.
Diuresis and swelling
Hydrochlorothiazide is the first choice (for GFR <30, replace furosemide)
Control urinary protein and high blood pressure
ACEI/ARB preferred
Urinary protein＜1g/d→BP＜130/80
Urinary protein≥1g/d→BP<125/75
Sodium restriction (<6g/d), water restriction, phosphorus restriction, protein restriction (0.6-1g/kg per day), fat restriction, and drug restriction
Active use of glucocorticoids and cyclophosphamide is not recommended
Differential diagnosis
Urology Overview
proteinuria
Physiological
Functionality: Appears during exercise and fever
Orthostatic: occurs when standing upright
Trace amount (30-300mg/d)
Diabetic nephropathy early stage
glomerular
Selectivity: mainly albumin
Non-selective: albumin, immunoglobulin, complement C3
Renal tubular (mostly <2g/d)
VitA binding protein, lysozyme, ribonuclease, light chain protein, β2-microglobulin
Small molecule protein: "Sister A kiss me"
secretory
Increased IgA excretion in urine
Organizational
Small molecule T-H glycoprotein in urine
Spillover
intravascular hemoglobin
Rhabdomyolysis of myoglobin
Hemangiomas of the Week/Agglutination/Free Immunoglobulin Light Chains
hematuria
Urinary system inflammation, stones, tumors, etc.
Gross hematuria: >1ml blood/1L urine (meat-washing water sample)
Microscopic hematuria
Urinary sediment red blood cells >3/HP
12h urine red blood cells＞5×10^5
Contrast: Pyuria (urinary tract infection)
WBC＞5/HP
12h urine white blood cells＞10^6
glomerular hematuria
Phase contrast microscopy shows a large number of deformed red blood cells (normally morphological red blood cells may appear in rapidly progressive nephritis)
The asymmetric volume distribution curve of urinary red blood cells and the peak value of the curve are smaller than the peak venous red blood cell volume.
May be accompanied by red blood cell casts and massive proteinuria
Cast urine
red blood cell casts
glomerular disease
white blood cell casts
Pyelonephritis
kidney immune response
Waxy casts (poor prognosis)
Long-term blockage of the kidneys (kidney failure)
Severe deformation of renal tubules
epithelial cell casts
tubular necrosis
fat casts
Fatty deformation of renal tubular epithelium, etc. (nephrotic syndrome)
Partial renal function test (different from total renal function)
Intravenous pyel/urography IVP/IVU
CT urography CTU
Radionuclide renal scintigraphy (renogram)
renal blood flow
Kidney anatomy and function
Is there any obstruction?