Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
NEPHROLOGY
Initial clinical and laboratory data base for defining major syndromes in nephrology
Syndromes
Important clues to diagnosis
Findings which are common but
not of diagnostic value
Acute or rapidly
Anuria, oliguria
Hypertension, hematuria
progressive renal
Documented recent decline in GFR
Proteinuria, pyuria
failure
Casts, edema
Acute nephritis
Hematuria, RBC casts, azotemia,
Proteinuria, pyuria
oliguria, edema, hypertension
Circulatory congestion
Chronic renal failure Azotemia for > 3 months
Hematuria, proteinuria
Prolonged symptoms or signs of
Casts, oliguria
uremia; Symptoms or signs of renal
Polyuria, nocturia
osteodystrophy
Edema, hypertension
Kidneys reduced in size bilaterally
Electrolyte disorders
Broad casts in urinary sediment
Nephrotic syndrome Proteinuria > 3.5 g per 1.73 m2 per
Casts
Edema
24 h, hypoalbuminemia,
hyperlipidemia, lipiduria
Asymptomatic
Hematuria, proteinuria (below
urinary
nephrotic range)
abnormalities
Sterile pyuria, casts
Urinary tract
Hematuria
Bacteriuria >105 colonies/ml
infection
Other infectious agent documented in Mild azotemia
Mild proteinuria
urine. Pyuria, leukocyte casts
Fever
Frequency, urgency
Bladder tenderness, flank tenderness
Renal tubule defects Electrolyte disorders
Hematuria "Tubular" proteinuria
Polyuria, nocturia
Enuresis
Symptoms or signs of renal
osteodystrophy
Large kidneys
Renal transport defects
Hypertension
Systolic/diastolic hypertension
Proteinuria, casts, azotemia
Nephrolithiasis
Previous history of stone passage or
Hematuria
removal
Pyuria
Previous history of stone seen by xFrequency, urgency
ray
Renal colic
Urinary tract
Azotemia, oliguria, anuria
Hematuria
obstruction
Polyuria, nocturia, urinary retention
Pyuria
Slowing of urinary stream
Enuresis, dysuria
Large prostate, large kidneys
Flank tenderness, full bladder after
voiding
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Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
GLOMERULAR DISEASE
Glomerulus: afferent arteriole – capillary bed – efferent arteriole, mesangium,
cell types: podocyte (glomerular epithelial cell), endothelial cell, mesangial cell,
parietal epithelial cell
The podocytes support the glomerular basement membrane (GMB)
Pathologic features of glomerular disease
focal
some (but not all) glomeruli contain the lesion
diffuse (global)
most glomeruli (>75%) contain the lesion
segmental
only a part of the glomerulus is affected by the lesion (most
focal lesions are also segmental)
proliferation
an increase in cell number due to hyperplasia of one or
more of the resident glomerular cells with or without
inflammatory cell infiltration
membrane
capillary wall thickening due to deposition of immune
alterations
deposits or alterations in basement membrane
crescent formation epithelial cell proliferation and mononuclear cell
infiltration in Bowman‘s space
2/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
Mechanisms of glomerular injury
Glomerular antibody deposition
Sensitized cells
Complement
C5b-9
C5a
Glomerular epithelial cells Neutrophils, platelets Macrophages
Mesangial
cells
Oxidants – Proteases
Consequences
of injury
Proteinuria
Glomerular sclerosis
Interstitial fibrosis
Renal failure
Glomerular syndromes
acute nephritic syndrome
nephronal hematuria temporally associated with
acute renal failure
rapidly progressive
nephronal hematuria with renal failure
glomerulonephritis
developing over weeks to months and diffuse
glomerular crescent formation
nephrotic syndrome
massive proteinuria (>3.5 gm/day/1.73 m2) with
variable edema, hypoalbuminemia,
hyperlipidemia and hyperlipiduria
with „bland sediment“ „pure“ nephrotic syndrome
with „active“ sediment „mixed“ nephrotic/nephritic syndrome
asymptomatic urinary
isolated proteinuria (usually <2 gm/day)
abnormalities
or hematuria (with or without proteinuria)
3/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
Acute nephritic syndrome
abrupt onset (days) of hematuria and proteinuria temporally associated with
impairment of renal function (e.g., oliguria, rise in BUN, creatinine, retention of
salt and water resulting in the development of hypertension)
Causes of acute glomerulonephritis
Infectious diseases
A
Poststreptococcal glomerulonephritisa
B
Nonstreptococcal postinfectious glomerulonephritis
1
Bacterial: infective endocarditis,a "shunt nephritis," sepsis,a pneumococcal
pneumonia, typhoid fever, secondary syphilis, meningococcemia
2
Viral: hepatitis B, infectious mononucleosis, mumps, measles, varicella,
vaccinia, echovirus, and coxsackievirus
3
Parasitic: malaria, toxoplasmosis
Multisystem diseases: systemic lupus erythematosus,a vasculitis,a Henoch-Schonlein purpura,a
Goodpasture's disease
Primary glomerular diseases: membranoproliferative glomerulonephritis, Berger's disease (IgA
nephropathy),a "pure" mesangial proliferative glomerulonephritis
Miscellaneous: Guillain-Barre syndrome, radiation of Wilms's tumor, diphtheria-pertussis-tetanus
vaccine, serum sickness
a Most common causes.
Differential diagnosis of acute nephritic syndrome
low serum complement level
normal serum complement level
acute postinfectious
IgA nephropathy
glomerulonephritis
idiopathic rapidly progressive
membranoproliferative
glomerulonephritis
glomerulonephritis
anti-GBM disease
systemic lupus erythematosus
polyarteritis nodosa
subacute bacterial endocarditis
Wegener‘s granulomatosis
visceral abscess
Henoch-Schönlein purpura
„shunt“ nephritis
Goodpasture‘s syndrome
cryoglobulinemia
4/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
Poststreptococcal glomerulonephritis
postinfection complication of nephritogenic strains of group A, beta-hemolytic
streptococcal infection
pharyngitis or streptococcal pyoderma as antecedent infection
most commonly children aged 3 to 12
Clin: malaise, cola-colored urine, mild hypertension, periorbital edema, nonnephrotic-range proteinuria
Lab: RBCs and RBC casts, leukocyturia and proteinuria on urinalysis
elevated ASLO titer
low serum complement
azotemia
Histol: diffuse proliferative (mesangial and endothelial cells) and exudative
(neutrophils and monocytes) GN with coarsely granular capillary loop deposits
of IgG and C3
Renal biopsy is indicated in adults only to establish the diagnosis
Th: there is no specific therapy; antibiotics should be administered if cultures are
positive for Streptococcus. Salt restriction, diuretics and antihypertensive agents
may be required
Complete recovery occurs in 90% of patients. Minor urinary sediment
abnormalities may occur for several years in some patients. progression to
chronic renal failure is very rare.
Fewer than 5% of patients have oliguria for more than 7 to 9 days, and the
prognosis in these patients is less favorable.
Nonstreptococcal postinfectious glomerulonephritis may occur after bacterial
(staphylococcal, pneumococcal), viral (mumps, hepatitis B, varicella, coxsackie,
infectious mononucleosis), protozoal (malaria, toxoplasmosis) and other
infections (schistosomiasis, syphilis).
Glomerulonephritis associated with infective endocarditis
(usually a mild form of acute nephritic syndrome)
Rapidly progressive glomerulonephritis
= a syndrome characterized by nephronal hematuria with renal failure
developing over weeks to months and diffuse glomerular crescent formation
Types of rapidly progressive glomerulonephritis (RPGN)
anti-GM antibody-mediated RPGN
- idiopathic
- Goodpasture‘s syndrome
- associated with other primary glomerular diseases
5/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
immune complex-mediated RPGN
- idiopathic
- associated with other primary glomerular diseases
membranoproliferative glomerulopathy
IgA nephropathy
- associated with secondary glomerular diseases
postinfectious glomerulonehpritides
systemic lupus erythematosus
non-immune-mediated RPGN
idiopathic pauci-immune RPGN (ANCA associated)
systemic vasculitides (polyarteritis nodosa, Wegener‘s granulomatosis)
Causes of rapidly progressive glomerulonephritis
INFECTIOUS DISEASES
A
Poststreptococcal glomerulonephritisa
B
Infective endocarditisa
Occult visceral sepsis
Hepatitis B infection (with vasculitis and/or cryoimmunoglobulinemia)
C
D
MULTISYSTEM DISEASES
A
Systemic lupus erythematosusa
B
C
D
Henoch-Schonlein purpuraa
Systemic necrotizing vasculitis (including Wegener's granulomatosis) and
microscopic polyarteritisa
Goodpasture's diseasea
Essential mixed (IgG/IgM) cryoimmunoglobulinemia
Malignancy
Relapsing polychondritis
Rheumatoid arthritis (with vasculitis)
E
F
G
H
DRUGS
A
Penicillaminea
B
C
D
A
Hydralazine
Allopurinol (with vasculitis)
Rifampin
Idiopathic or primary crescentic glomerulonephritisa
1
Type Iwith linear deposits of Ig (anti-glomerular basement
membrane antibody-mediated)
2
Type IIwith granular deposits of Ig (immune-complex-mediated)
3
Type IIIwith few or no immune deposits of Ig ("pauci-immune")
a Antineutrophil-cytoplasmic-antibody-associated (renal-limited
microscopic polyarteritis)
b Antineutrophil-antibody-negative
4
Type IVcombinations of types I and IIIa
6/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
B
Superimposed on another primary glomerular disease
1
Mesangiocapillary (membranoproliferative glomerulonephritis)a
2
Membranous glomerulonephritisa
Berger's disease (IgA nephropathy)a
a Most common
Therapy:
Anti-GMB GN: high-dose oral prednisone in concert with plasma exchange
Immune complex RPGN: treat underlying condition
Non-immune-mediated RPGN: cyclophosphamide and steroids
Nephrotic syndrome
presence of proteinuria > 3.5 gm/24 hr/1.73 m2, hypoalbuminemia, edema,
hyperlipiduria, and hyperlipidemia
Glomerulopathies associated with nephrotic syndrome
nephrotic-range proteinuria with „bland“ urine sediment (pure nephrotic)
primary glomerular disease
minimal change nephrotic syndrome (lipoid nephrosis)
membranous glomerulopathy
focal glomerulosclerosis
secondary glomerular disease
diabetic nephropathy (Kimmelstiel-Wilson glomerulosclerosis)
amyloidosis
nephrotic-range proteinuria with „active“ urine sediment („mixed“,
nephrotic/nephritic)
primary glomerular disease
membranoproliferative glomerulopathy
secondary glomerular disease
membranoproliferative glomerulopathy
systemic lupus erythematosus
Henoch-Schönlein purpura
mixed essential cryoglobulinemia
Causes of the nephrotic syndrome
PRIMARY GLOMERULAR DISEASESa
A
Minimal change diseasea
B
C
D
E
Mesangial proliferative glomerulonephritisb
Focal and segmental glomerulosclerosisa
Membranous glomerulonephritisa
Membranoproliferative glomerulonephritisa
7/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
F
Other uncommon lesions
1
Crescentic glomerulonephritis
2
Focal and segmental proliferative glomerulonephritis
3
Fibrillary and/or immunotactoid glomerulonephritis
SECONDARY TO OTHER DISEASES
A
Infections: poststreptococcal glomerulonephritis,a endocarditis, "shunt
nephritis," secondary syphilis, leprosy, hepatitis B,a HIV infection and
AIDS, infectious mononucleosis, malaria, schistosomiasis, filariasis
B
Drugs: organic gold; inorganic, organic, and elemental mercury;
penicillamine; "street" heroin, nonsteroidal anti-inflammatory agents,a
probenecid; captopril; Tridione; mesantoin; perchlorate; antivenom;
antitoxins; contrast media
C
Neoplasia: Hodgkin's disease, lymphomas, leukemia, carcinomas,
melanoma, Wilms's tumor
D
Multisystem: systemic lupus erythematosus,a Henoch-Schonlein purpura,a
vasculitis, Goodpasture's disease, dermatomyositis, dermatitis herpetiformis,
amyloidosis,a sarcoidosis, Sjogren's syndrome, rheumatoid arthritis, mixed
connective tissue disease
E
Heredofamilial: diabetes mellitus,a Alport's syndrome, sickle cell disease,
Fabry's disease, nail-patella syndrome, lipodystrophy, lecithin-cholesterol
acyltransferase deficiency, congenital nephrotic syndrome
F
Miscellaneous: preeclamptic toxemia, thyroiditis, myxedema, malignant
obesity, renovascular hypertension, chronic interstitial nephritis with
vesicoureteric reflux, chronic allograft rejection,a bee stings
a Most common.
b Includes Berger's disease (IgA nephropathy)
Minimal change nephrotic syndrome (lipoid nephrosis)
sudden onset of nephrotic syndrome in children aged 2 – 6 years
Lab: normal renal function, normal complement levels
Histol: light microscopy is normal; EM: fusion of the foot processes
Spontaneous remission in ~ 50% of patients
Th: prednisone 60 mg/m2/day in children and 1.5 – 2 mg/kg/day in adults; at 4
weeks, alternate-day therapy is begun for 4 more weeks, with a tapering regimen
given over the next 4 – 6 months. Relapsers or steroid-dependent patients may
benefit from adjunctive therapy with alkylating agents (cyclophosphamide,
chlorambucil).
About 75% of patients are disease free at 10 years, with a 10-year survival rate
of 95%.
8/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
Focal glomerulosclerosis
FGS accounts for 10 – 15% of children and 15 to 20% of adults with idiopathic
nephrotic syndrome.
Etiology: idiopathic
secondary (heroin, AIDS, reflux nephropathy)
Lab: nephrotic-range proteinuria with „bland“ urinary sediment
Azotemia, microscopic hematuria are frequent
Histol: focal and segmental collapse of capillary loops and mesangial sclerosis
with hyaline droplets
~ 30% of patients respond to steroid therapy with a lasting remission, but most,
particularly those with persistent nephrotic syndrome, progress to chronic renal
failure (55% by 10 years).
Rcurrence of FGS in transplants occurs in as many as 40% of patients
Membranous glomerulopathy
Slowly progressive course with remissions and exacerbations;
spontaneous complete remission in as many as ~ 25% of patients
50% progress to end-stage renal failure by 5 – 10 years
Th: children and adults with low proteinuria need not receive specific treatment.
Patients with severe proteinuria and older men are treated with prednisone and
chlorambucil
Diabetic nephropathy
Prevalence of nephropathy is 30 to 50% in IDDM and 10 to 15% in NIDDM.
Def.: a clinical syndrome characterized by persistent albuminuria (>300 mg/24
hr), decline in GFR, and raised arterial blood pressure. DN is rare during the
first 5 years of DM, it peaks at ~ 15 years of DM.
Microalbuminuria (> 30 mg and < 300 mg/day) strongly predicts the
development of diabetic nephropathy.
The rate at which patients with proteinuria progress is highly variable.
Kimmelstiel-Wilson nodular glomerulosclerosis is found in only 15 – 20% of
patients with diabetic nephropathy. More common is diffuse glomerulosclerosis
(increase in hyaline material within the mesangial areas surrounded by dilated
and thickened capillary loops.
Th: vigorous control of blood sugar, antihypertensive treatment, restriction of
dietary proteins. ACE inhibitors have marked antiproteinuric effect and probably
are indicated even in the face of normal blood pressure.
9/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
Amyloidosis
Four types of systemic amyloidosis:
- primary – a plasma cell dyscrasia, most common
- secondary – develops after chronic inflammatory or infectious disease
- hereditary – several autosomal dominant hereditary forms
- dialysis associated
Nephrotic syndrome is the initial feature in 75% of patients with secondary
amyloidosis and in 25% of patients with primary amyloidosis.
Dg: by tissue biopsy
Th: no specific treatment; in primary amyloidosis, colchicine, melphalan, and
prednisone have been used.
Nephrotic syndrome with „active“ urine sediment
Membranoproliferative glomerulopathy
A disease of young people.
~ 50% present with nephrotic syndrome, 25 – 30% with asymptomatic
proteinuria, and 15 – 20% with acute nephritic syndrome. Hematuria and
proteinuria are almost always present.
Serum C3 levels are depressed in > 70% of patients.
Histol.: thickening of capillary loops and mesangial hypercellularity
Course: slow but progressive; ~ 30% of patients are in chronic renal failure by
10 years
Th: steroids + cytotoxic drugs but effects are poor
Systemic lupus erythematosus (SLE) GN
SLE accounts for ~ 5 – 10% of patients with nephrotic syndrome
Dg: antinuclear antibody in the presence of inflammation of multiple organs
Renal disease is present clinically in up to 90% of patients with SLE; all patients
have renal injury on renal biopsy.
Serum complement levels are usually low.
Histologic types: mesangial, focal proliferative, diffuse proliferative,
membranous.
Th: the lowest possible dose of steroids; in diffuse proliferative type steroids +
cytotoxic drugs
Henoch-Schönlein purpura
Most often in children: purpuric lesions on the buttocks and legs, episodic
abdominal pain, arthralgias, fever, malaise, proteinuria with hematuria and RBC
casts. Serum C3 levels are normal.
Histol.: mesangial hypercellularity and crescent formation
Course: usually self-limited, disappearing after a few months or years. About
10% of patients progress to ESRD.
Th: ineffective
10/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
Essential mixed cryoglobulinemia
Mixed cryoglobulins are composed of monoclonal IgM rheumatoid factor and
polyclonal IgG.
Clin: palpable purpura, fever, Raynaud’s phenomenon, arthralgias, and
weakness.
Renal manifestations are seen in 40 – 50% of patients and vary from proteinuria
and/or hematuria to acute nephritic syndrome
Histol: diffuse proliferative glomerulonephritis with intraluminal hyaline
thrombi.
~ 50% of patients have underlying chronic hepatitis C virus infection → all
patients should be screened for the presence of hepatitis C.
Th: treat hepatitis C, plasmapheresis to decrease the circulating cryoprecipitates
Asymptomatic urinary abnormalities
Isolated proteinuria
proteinuria without hematuria
postural proteinuria
Isolated hematuria (with or without proteinuria)
IgA nephropathy
hereditary nephritis
Alport’s syndrome
thin basement membrane disease
benign recurrent hematuria
IgA nephropathy
is found in up to 50% of patients with asymptomatic hematuria.
It is the most common cause of primary glomerular disease in Europe and USA.
Clin: gross hematuria following a viral illness, other patients present with
asymptomatic hematuria with mild to moderate proteinuria. Most patients are
between 15 and 35. Serum complement is normal.
Histol: mesangial hypercellularity, segmental sclerosis, crescent formation,
tubular atrophy, and interstitial fibrosis. Mesangial deposits of IgA are
characteristic.
Course: progressive renal insufficiency develops in 20 to 30% of patients after
20 years. Some have a more rapid progression.
No effective therapy is available.
Hereditary nephritis (Alport’s syndrome)
Usually presents in childhood with recurrent gross hematuria. Mild proteinuria
is often present, but nephrotic syndrome is rare.
Deafness is present in ~ 50% of patients.
Males are usually more affected than females and often develop renal failure by
age of 30.
11/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
Histol: nonspecific interstitial foam cells, immunofluorescence is negative for
immunoglobulins and complement.
Th: no effective treatment is available.
Chronic glomerulonephritis
is the culmination of many different glomerular diseases associated with the
progressive loss of functioning nephrons.
These patients generally progress to ESRD.
DISEASES OF THE RENAL INTERSTITIUM
Tubulointerstitial nephropathy encompasses a group of clinical disorders that
affect the renal tubules and interstitium principally, with relative sparing of the
glomeruli and renal vasculature. Two principal categories:
1. Acute interstitial nephritis – rapid decline in renal function (days to weeks)
2. Chronic interstitial nephropathy
Transport dysfunctions of tubulointerstitial disease
Defect
Cause(s)
Reduced GFRa
Fanconi syndrome or competent
defects
Hyperchloremic acidosisa
Tubular or small-molecular-weight
proteinuriaa
Polyuria, isothenuriaa
Hyperkalemiaa
Salt wasting
Obliteration of vasculature and obstruction
of tubules
Damage to proximal tubular reabsorption of
glucose, amino acids, phosphate, and
bicarbonate
1.
Reduced ammonia production
2.
Inability to acidify the collecting
duct fluid (distal renal tubular
acidosis)
3.
Proximal bicarbonate wasting
Failure of proximal tubule protein
reabsorption
Damage to medullary tubules and
vasculature
Potassium secretory defects including
aldosterone resistance
Distal tubular damage with failure of sodium
reabsorption
a Common
12/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
Principal causes of tubulointerstitial disease of the kidney
TOXINS
Exogenous toxins
Analgesic nephropathya
Lead nephropathy
Miscellaneous nephrotoxins (e.g., antibiotics, cyclosporine, radiographic
contrast media, heavy metals)a,b
Metabolic toxins
Acute uric acid nephropathy
Gouty nephropathy a
Hypercalcemic nephropathy
Hypokalemic nephropathy
Miscellaneous metabolic toxins (e.g., hyperoxaluria, cystinosis,
Fabry's disease)
NEOPLASIA
Lymphoma
Leukemia
Multiple myeloma a
IMMUNE DISORDERS
Hypersensitivity nephropathya,b
Sjogren's syndrome
Amyloidosis
Transplant rejection b
Tubulointerstitial abnormalities associated with glomerulonephritis
AIDS
VASCULAR DISORDERS
Arteriolar nephrosclerosisa
Atheroembolic disease
Sickle cell nephropathy
Acute tubular necrosisa,b
HEREDITARY RENAL DISEASES
Hereditary nephritis (Alport's syndrome)
Medullary cystic disease
Medullary sponge kidney
Polycystic kidney disease
13/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
INFECTIOUS INJURY
Acute pyelonephritisa,b
Chronic pyelonephritis
MISCELLANEOUS DISORDERS
Chronic urinary tract obstruction a
Vesicoureteral refluxa
Radiation nephritis
a Common. b Typically acute.
Acute interstitial nephritis
is a clinicopathologic syndrome that is characterized by the sudden onset of
clinical signs of renal dysfunction associated with a prominent inflammatory cell
infiltrate within the renal interstitium. AIN accounts for 10 – 20% of acute renal
failure cases.
Causes of acute interstitial nephritis
Drug related
antimicrobial drugs
penicillins (esp. methicillin)
rifampin
sulfonamides
ciprofloxacin
cephalosporins
NSAIDs
allopurinol
sulfonamide diuretics
Systemic infections
legionnaires disease
leptospirosis
streptococcal infections
cytomegalovirus
infectious mononucleosis
Primary renal infections
acute bacterial pyelonephritis
Immune disorders
transplant rejection
systemic lupus erythematosus
Idiopathic
Clin: the major clinical manifestation of AIN is the development of acute renal
insufficiency. Hypertension and edema are uncommon in AIN.
Lab: hematuria, often macroscopic, is common when AIN is caused by drugs, as
are sterile pyuria and leukocyte casts.
Eosinophilia is highly suggestive of AIN.
Mild to moderate proteinuria is common.
14/15
Nephrology - Seminar 1
Seminars from internal medicine for the 5th year
Prof. Jiří Horák
Th: discontinue the offending drug; treat underlying infection; a short course of
high-dose prednisone (1 mg/kg/day) may accelerate recovery.
Chronic tubulointerstitial nephropathy
Sy: Progressive renal insufficiency, non-nephrotic range proteinuria, and
functional tubular defects.
Histol: interstitial fibrosis with atrophy and loss of renal tubules.
It is responsible for 15 – 30% of all end-stage renal disease.
Clinical findings in chronic tubulointerstitial disease
hyperchloremic metabolic acidosis
hyperkalemia
reduced maximal urinary concentrating ability
partial or complete Fanconi’s syndrome
phosphaturia
bicarbonaturia
aminoaciduria
uricosuria
glycosuria
urinalysis
may be normal or may contain cellular elements; absence
of RBC casts
modest proteinuria (<2 gm/day)
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