CKD pt 2 Flashcards
(145 cards)
1
Q
2 categories of processes that lead to abnormal glomerular function
A
- nephritic spectrum
- nephrotic spectrum
2
Q
Urine sediment with hematuria, +/- RBC casts
Proteinuria (< 3 g/d)
inflammation/immune is often involved
what type of glomerular disease?
A
nephritic
3
Q
“Bland” urine sediment - no cells or casts
May see oval fat bodies
Proteinuria (at least 300 mg/d, often > 3 g/d)
what type of glomerular disease
A
nephrotic
4
Q
Broad term for glomerular diseases in the nephritic spectrum
Generally - inflammatory process affecting glomeruli, causing renal dysfunction
A
Glomerulonephritis
5
Q
causes of glomerulonephritis
A
- Immune complex deposition
- Pauci-immune
- Anti-glomerular basement membrane
- C3 glomerulopathy
- Monoclonal Ig
6
Q
causes of immune complex deposition in CKD
A
IgA nephropathy (Berger disease), infections, endocarditis, lupus nephritis, membranoproliferative (MPGN), cryoglobulinemic (seen with HCV)
7
Q
what specific pathogen is associated particularly in immune complex deposition glomerulonephritis
A
strep infections
8
Q
pt comes in with edema, HTN and smoky colored urine
what could they possibly have?
A
glomerulonephritis
9
Q
labs seen in glomerulonephritis
CKD
A
- sCr rises over days - months - BUN:Cr ratio primary helpful to assess volume
- Urinalysis - hematuria, moderate proteinuria (usually < 3 g/d)
- Urine sediment - RBCs, WBCs, RBC casts
- RBCs dysmorphic from crossing damaged glomerulus
- RBC casts - sign of heavy glomerular bleeding, tubular stasis
10
Q
additional lab findings for glomerulonpehritis
CKD
A
- Complement levels - may be low in C3 complex and immune complex glomerulonephritis (except Berger’s disease)
- ASO titers - help evaluate for recent streptococcal infection
- anti-GBM antibodies
- P-ANCA and C-ANCA levels - pauci-immune glomerulonephritis
- SPEP - monoclonal gammopathies
- Inflammatory markers - ESR, CRP, ANA
11
Q
what could reveal patterns of inflammation related to cause of glomerulonephritis
not commonly done
A
Renal biopsy - consider if no CI (bleeding disorder, uncontrolled HTN)
12
Q
tx for glomerulonephritis
CKD
A
- Management of HTN
- Management of volume overload - if present
- Antiproteinuric therapy (ACE/ARB) - if no AKI
- Immunosuppressive agents - High-dose corticosteroids, Cytotoxic agents may be used
- Plasma exchange - Goodpasture disease, Pauci-immune
13
Q
Postinfectious Glomerulonephritis is usually due to ?
A
GABHS - Often after pharyngitis or impetigo
May occur with other bacteria, viral (Hep B/C, CMV, EBV), syphilis, malaria, fungal
14
Q
s/s of Postinfectious Glomerulonephritis
A
1-3 wks after infection, avg. 7-10 d
S/S - vary from asx hematuria to nephritic syndrome
15
Q
Pt with recent GABHS infection presents with
Serum - Low complement; high ASO titer (unless previous abx)
Urine - hematuria, subnephrotic proteinuria (< 3 g/d), RBC casts
what could this patient might have?
A
Postinfectious Glomerulonephritis
16
Q
a renal biopsy comes back with “humps” of immune complex deposits. what is the dx?
A
Postinfectious Glomerulonephritis
17
Q
tx for Postinfectious Glomerulonephritis? What medication is NOT recommended due to not improving outcome?
A
tx infection
Supportive - antihypertensives, salt restriction, diuretics
Steroids do not generally improve outcome
18
Q
Most common primary glomerular disease worldwide
A
IgA Nephritis (Berger’s Disease)
Can be primary (renal-limited) or secondary to cirrhosis, celiac disease, HIV, CMV
19
Q
IgA Nephritis (Berger’s Disease)
is MC in who?
A
males
children and young adults
20
Q
10 yr old male pt comes in with an episode of gross hematuria and URI, what is their probable dx?
A
IgA Nephritis (Berger’s Disease)
Often in conjunction with mucosal viral infection (i.e., URI)
21
Q
lab findings of IgA Nephritis (Berger’s Disease)
A
Serum - Normal complement; no confirming serum test
Urine - hematuria (micro or gross), proteinuria (varies)
22
Q
tx for IgA Nephritis (Berger’s Disease)
A
- varies depending on risk for progression
- Low risk - no HTN, normal GFR, minimal proteinuria - monitor yearly
- High risk - proteinuria >1.0 g/d, decreased GFR, HTN - ACE or ARB
23
Q
Systemic small-vessel vasculitis - MC systemic vasculitis of childhood
A
Henoch-Schönlein Purpura
24
Q
Associated with IgA deposition in vessel walls
Often associated with inciting infection (such as GABHS)
More common in males; more common in children
A
Henoch-Schönlein Purpura
25
Palpable purpura in lower extremities and butocks; arthralgias, abdominal symptoms (nausea, colic, melena)
what is this dx
Henoch-Schönlein Purpura
26
what lab findings would you find with Henoch-Schönlein Purpura
Serum - Normal complement; no confirming serum test
Urine - hematuria , proteinuria (varies)
27
tx for Henoch-Schönlein Purpura
no direct treatment proven successful
Supportive care - hydration, rest, pain relief
28
MCC of nephrotic glomerular disease
DM
29
what is the “Nephrotic range” proteinuria?
| value
>3 g/d
30
s/s of Subnephrotic proteinuria
asx
31
s/s of Nephrotic Syndrome
peripheral edema
* May be in dependent regions
* May be generalized (including periorbital edema)
* Dyspnea, pleural effusions, ascites can occur
32
oval fat bodies
grape clusters (light microscopy)
maltese crosses (polarized light)
are seen in what glomerular disease
nephrotic syndrome
33
what urinalysis could you do for nephrotic syndrome
dipstick - only detects albumin
spot urine protein:urine Cr ratio
24-hr urine for protein
34
serum labs of nephrotic syndrome
* depends on amount of protein lost
* Hypoalbuminemia - < 3 g/dL
* Hypoproteinemia - < 6 g/dL
* Hyperlipidemia - >50% of early nephrotic pts (hypertriglyceridemia)
* Elevated ESR - due to altered plasma components
* Possible deficiencies - Vitamin D, zinc, copper deficiency
35
an adult pt has a new onset idiopathic nephrotic syndrome, what could you do?
renal bx
Rarely done if long-standing DM or other obvious cause is present
36
tx for nephrotic syndrome
1. _Protein restriction_ - if subnephrotic/mild
- If > 10 g/d lost - INCREASE protein instead
- **ACE/ARB** - lower urine protein excretion by reducing glomerular capillary pressure; antifibrotic effects
2. _Edema_ - dietary salt restriction; diuretics
- **Thiazide, loops** - _larger doses needed_
3. _Hyperlipidemia_ - diet and exercise; **lipid-lowering rx**
4. _Hypercoagulability_ - **anticoagulation**
- seen if serum albumin < 2 g/dL
- Anticoag x **3-6 months min**. if evidence of thrombosis
- Ongoing - if renal vein thrombosis, PE, recurrent thromboemboli
37
why do we see hypercoagulability in nephrotic syndrome
**Urinary loss of antithrombin, protein C, protein S**
increased platelet activation
38
MCC proteinuric renal disease in children
Minimal Change Disease
## Footnote
20-25% of primary nephrotic disease in adults
39
s/s of minimal change disease
* often full-blown nephrotic syndrome
* Thromboembolic events, hyperlipidemia, protein malnutrition
40
tx for minimal change disease
**Corticosteroids** - **Prednisone**, 60 mg/m2/d
* < 8 wks for children, < 16 wks for adults
* Continue for several wks after proteinuria remission
* Taper dose after course is complete
41
MCC primary nephrotic syndrome in adults
Membranous Nephropathy
42
causes of Membranous Nephropathy
Due to immune complex deposition
May be secondary to carcinoma, HBV, HCV, syphilis, endocarditis, autoimmune disease, NSAIDs, captopril
43
pt comes in with edema and frothy urine. other than those he is asx, what could be their condition?
Membranous Nephropathy
44
membranous nephropathy have a Higher risk of hypercoagulable state, esp. where?
renal vein thrombosis
45
tx for Membranous Nephropathy
ACE/ARB, immunosuppressive agents, transplant
46
Extracellular deposition of amyloid protein
Proteinuria, decreased GFR, nephrotic syndrome
what is this dx
Amyloidosis
47
pt comes in with some inflammation and palpable kidneys
no abd or flank pain
what could be thier dx
**Amyloidosis**
Kidneys are often enlarged
May see other chronic
inflammatory dz
Treatment - limited options
48
MC cause of ESRD in the US
Diabetic Nephropathy
20 year risk: About 40% (higher risk in T2DM)
49
Diabetic Nephropathy usually develop when after DM onset?
10 yrs
50
presentation of diabetic nephropathy
* Early - hyperfiltration with increased GFR
* Later - microalbuminuria (30-300 mg/d)
* Progression - albuminuria 300+ mg/d
51
when to tx diabetic nephropathy
as soon as microalbuminuria is found
52
Disorders mainly affecting renal tubules and interstitium
Tubulointerstitial Disease
53
difference between acute vs chronic Tubulointerstitial Disease
1. **Acute - Acute Interstitial Nephritis**
* Presents with acute renal failure
* 70% - due to **meds**
2. **Chronic - more indolent onset**
* May manifest with tubular dysfunction
* Predominant pathology - interstitial fibrosis, tubular atrophy
54
causes of chronic tubulointerstitial disease
* **Obstructive Uropathy - MCC**
* **Vesicoureteral Reflux - 2nd MCC**
* Analgesic Nephropathy - ingest min 1 g/d for 3+ yrs
* May also be due to renal ischemia, glomerular disease
55
causes of obstructive uropathy
Prolonged obstruction of urinary tract
* Prostatic disease
* Ureteral calculi
* Cancer of cervix, colon, or bladder
* Retroperitoneal tumors or fibrosis
56
how does obstructive uropathy cause damage?
Backflow of urine → extravasation into interstitium → inflammation, fibrosis
Prolonged reflux of urine causes damage, scarring
57
obstructive uropathy s/s
_vary with underlying cause, location/degree of obstruction_
* Hydronephrosis - asx
* Pain - if acute complete obstruction (e.g., stone)
* Bladder distension - +/-
* HTN - +/-
* Urine output - +/-
* May present with oliguria or anuria
* May present with polyuria
58
UA and serums of obstructive uropathy
often benign; may see hematuria, pyuria
Serum creatinine - typically elevated
59
Imaging shows dilation of collecting system
what is the dx
Obstructive Uropathy
60
when should imaging be done with kidney disease? (Acute and chronic)
all pts with AKI of unknown cause
all CKD pts to r/o obstruction
61
preferred imaging study for obstructive uropathy? what other imagings can be done
US - preferred imaging study
CT - more detailed information, not first-line
If suspected stone, PCKD - noncontrast CT
62
tx for Obstructive Uropathy
**relief of obstruction ASAP**
Prolonged obstruction → further tubular damage, especially in distal nephron
Longstanding obstruction → renal scarring
63
Vesicoureteral Reflux is MC in who?
children
| Primarily occurs during childhood
64
cause of Vesicoureteral Reflux
Incompetent, misplaced vesicoureteral sphincter → retrograde flow of urine while voiding
Inflammatory response and scarring
65
child with hx of UTIs comes in with complaint of a UTI. what could be their dx?
Vesicoureteral Reflux
Especially young children with history of recurrent UTIs
Adults may give hx of frequent UTIs
66
Vesicoureteral Reflux may not be dx until later in life until when?
HTN and proteinuria develop
67
presentation of vescoureteral reflux (s/s, labs, urine)
* S/S - HTN, hx of frequent UTIs
* Labs - varying elevations in BUN/Cr
* Urine - mild-moderate proteinuria, no sediment unless current infection
68
imaging of choice for vesicoureteral reflux
**Voiding cystourethrogram** - radiopaque dye instilled in bladder; pt then voids while x-ray is taken
69
upon US what would be seen with vesicoureteral reflux? what 3 things could be found in an adult?
hydronephrosis, renal scarring
Adults - asymmetric small kidneys
* irregular outlines
* thin cortices
* areas of compensatory hypertrophy
70
tx for Vesicoureteral Reflux
* Maintaining sterile urine in childhood - Reduces severity of scarring
* Surgical reimplantation of ureters - for children with persistent high-grade reflux - Ineffective in adolescents/adults
* Control of HTN - ACE/ARB
71
Usually seen in pts who ingest large amounts of analgesics
what type of chronic Tubulointerstitial Disease
Analgesic Nephropathy
72
what meds MC cause Analgesic Nephropathy
* phenacetin (banned in 1983)
* ASA, NSAIDs, acetaminophen
73
how much analgesics must be consumed to cause analgesic nephropathy?
at least 1 g/d for 3+ years
74
Analgesic Nephropathy
causes damage how?
* Tubulointerstitial inflammation and papillary necrosis
* Analgesics can be concentrated up to 10x higher in renal papillae > renal cortex
75
Urine presents hematuria, proteinuria, polyuria, pyuria
Sloughed papillae found
what is this dx
Analgesic Nephropathy
76
small, scarred kidney with papillary calcifications
seen on CT, what is the dx?
Analgesic Nephropathy
77
IVP shows contrast will fill area of sloughed papillae, causing a “ring shadow” or “golfball on a tee” sign
what is this dx
**Analgesic Nephropathy**
IVP rarely used due to risk of contrast nephropathy
78
tx for Analgesic Nephropathy
**DC of offending agent**
* Renal decline expected to progress if analgesics continued
* Renal function may stabilize or mildly improve if analgesic stopped in a timely manner
79
Autoimmune Interstitial Nephritis can be a complication of multiple autoimmune disorders:
* Amyloidosis
* Cryoglobulinemia
* IgA nephropathy
* Renal transplant rejection
* Anti-GBM-Antibody syndrome (Goodpasture syndrome)
* Sarcoidosis
* Sjogren Syndrome
* SLE
80
vary with underlying cause; may have no s/s
Polyuria, decreased urinary concentrating ability
Volume depletion due to salt-wasting
Hyperkalemia
Hyperchloremic metabolic acidosis
what could this dx be?
Autoimmune Interstitial Nephritis
81
imaging reveals small, scarred kidneys, what could be the dx
Autoimmune Interstitial Nephritis
82
tx for autoimmune interstitial nephritis
controlling underlying cause
83
Deposition of calcium in renal parenchyma and tubules
what is the dx
**Nephrocalcinosis**
Can cause AKI, CKD
May also have normal renal function
Most pts do not progress to ESRD
84
cause of nephrocalcinosis
Caused by increase in urinary excretion of calcium, phosphate, and/or oxalate
**MCC - increased urinary calcium excretion**
85
risk for nephrocalcinosis
conditions that cause hypercalcemia, hyperphosphatemia, or increased excretion of calcium, phosphate or oxalate in urine
* **Hyperparathyroidism**
* **Vit D therapy**
* **Loops** (in high doses for a long period)
* Numerous other conditions
86
presentation of nephrocalcinosis
| s/s, labs, urine
* S/S - **asx MC** (incidental finding) - May see s/s of underlying cause
* Labs - possible hypercalcemia, hyperphosphatemia
* Urine - bland; may have sterile pyuria or hematuria
- Proteinuria, if present, usually < 500 mg/d
- 24-hr urine - increased Ca, phosphate, or oxalate
87
imaging of choice for nephrocalcinosis
US is modality of choice
Can also be visualized with CT
88
tx for nephrocalcinosis
correcting underlying metabolic disorder
89
65-70% (MC) of all renal masses
Single or Solitary Renal Cyst
90
where are most Single/Solitary Renal Cyst located?
**outer cortex, may be in medulla**
Often incidental US finding
Renal size usually normal
91
what signs are not present in Single or Solitary Renal Cyst
unlike most other kidney diseases?
HTN, signs of ESRD
not present
92
management for single/solitary renal cyst
1. If appears benign on imaging, routine follow up is acceptable management
* Refer to **Bosniak score**
* If develop after onset of dialysis → potential for adenocarcinoma
93
dx Medullary Cystic Kidney Disease during childhood is called what?
Juvenile Nephronophthisis
94
which Medullary Cystic Kidney Disease
are recessive and dominant
* Childhood (Juvenile NPH) - autosomal recessive
* Adult (MCKD) - autosomal dominant
95
Medullary Cystic Kidney Disease
forms where
**multiple small renal cysts at corticomedullary junction and in medulla**
Cortex becomes fibrotic → interstitial inflammation, glomerular sclerosis
96
presentation of medullary cystic kidney disease
Polyuria, pallor, lethargy, renal salt wasting
* HTN - later in disease
* Hyperuricemia can be present
* Juvenile NPH - growth restriction, ESRD < 20 yrs
* MCKD - ESRD ages 20-70
97
tx for Medullary Cystic Kidney Disease
adequate salt and water intake
No therapy to stop progression
Allopurinol if hyperuricemic
Does not recur in renal transplants
98
prevalence of Autosomal Dominant PKD
1 in 400 to 1 in 1000 pts
90% from autosomal dominant inheritance
99
2 genes of Autosomal Dominant PKD
1. ADPKD-1 - 85% of pts - more severe course
2. ADPKD-2 - 15% of pts - slower progression, later onset in life
100
presentation of Autosomal Dominant PKD
| s/s, PE, labs
_s/s_
* **abd or flank pain MC**
* **hx of UTI and nephrolithiasis**
* hx of HTN in >50 %
* Fhx of PKD in 75%
exam - large kidneys, may be palpable
Labs - hematuria (micro / gross), mild proteinuria - H&H tend to be maintained
101
what confirms ADPKD
**US confirms dx**; can use CT if unclear
* Age < 30 - 2+ renal cysts
* Age 30-59 - 2+ cysts in each kidney
* Age 60 + - 4+ cysts in each kidney
102
where else can cysts be found in ADPKD
40-50% have hepatic cysts
Cysts also often seen in spleen
103
tx for ADPKD (7)
1. _Pain_ -Bed rest, analgesics, cyst decompression
2. _Hematuria_ - Bed rest, hydration - resolves in ~ 1 wk
- Directed tx if sx of nephrolithiasis, UTI
- recurrent - possible RCC
3. _Nephrolithiasis_ - Pain control, hydration of 2-3 L/d
4. _HTN_ - ACE/ARB, Cyst decompression
5. _Cerebral aneurysms_ - Screening arteriography *not* recommended
6. _infected cyst_ - quinolones, TMP-SMZ
- May need 2 wks of IV tx then long-term oral abx
7. Avoidance of caffeine and protein
104
pain in ADPKD could be due to what
infection, bleeding into cysts, nephrolithiasis
105
hematuria in ADPKD could be due to what?
usually due to rupture of cyst
May also be due to kidney stone, UTI
106
what sx is MC in ADPKD (50% of pts at time of dx?)
HTN
107
about 20% of pts experience ____ in ADPKD
nephrolithiasis
108
10-15% of ADPKD have a cerebral aneurysm in what location?
circle of willis
109
pt with ADPKD exhibits flank pain, fever, ↑ WBC
what could this be? what is the work up?
infected cyst
CX - blood and urine may be +/-
CT scan - can help diagnose
110
what other complications can be seen in ADPKD
mitral valve prolapse, aortic aneurysms, aortic valve disease, colonic diverticula
111
what medication slows rate of change in kidney volume, lower rate of progression, reduces intracellular cyclic AMP
Vasopressin receptor antagonists
112
which Vasopressin receptor antagonist decreases cyst growth, has no improvements of kidney function?
Ocreotide
113
this Vasopressin V2 Receptor Antagonist slows renal decline
Tolvaptan (Jynarque, Samsca)
114
when is Tolvaptan recommended?
1. Recommended for all **pts 18+** with **GFR of 25+** mL/min and **1+ risk marker**:
* Mayo Class 1C, 1D, 1E
* Age ≤ 55 years and an eGFR < 65
* Kidney length > 16.5 cm in patient < 50 y/o
* PROPKD Score of > 6
115
which Tolvaptan is for ADPKD
Jynarque
116
which Tolvaptan is for hypervolemic/euvolemic hyponatremia
Samsca
117
dosing for Tolvaptan
45 mg in AM, 15 mg 8 hrs later (prior to 4 pm)
* Titrate up every 1-4 wks to max 90 mg AM and 30 mg PM
* Greater reduction in urinary osmolality = greater impairment of cyst growth
118
SE of Tolvaptan
thirst/polydipsia, polyuria/nocturia, **hypernatremia**, increased **liver enzymes**
119
BBW for Tolvaptan
should be initiated and reinitiated in patients **only in a hospital** where **serum sodium can be closely monitored**
120
CI of Tolvaptan
liver disease, pts on strong CYP3A4 inhibitors, allergy to rx
121
rare
Enlarged kidneys with small cysts on collecting tubules only
what is this dx
Autosomal Recessive PKD
122
presentation of Autosomal Recessive PKD
varies widely
* Enlarged kidneys (bilateral abdominal masses)
* Impaired urine concentration
* Metabolic acidosis
* HTN common
123
Up to 50% of neonates with ARPKD die from ____
pulmonary hypoplasia
## Footnote
Intrauterine kidney disease causes severe oligohydramnios
124
prognosis with ARPKD
80% of surviving neonates live to age 10 or longer
* **⅓ will develop ESRD by age 10**
* Many pts also develop portal hypertension from periportal fibrosis
125
diagnostics for ARPKD
**large, echogenic kidneys**
* Cysts visible only *after* birth
* **Absence of renal cysts in either parent** - helps distinguish ARPKD from ADPKD
126
tx for ARPKD
no specific therapy
Management of HTN
Dialysis and kidney transplant
127
renal artery stenosis is MC due to what
80-90% due to atherosclerotic occlusive disease
10-15% - fibromuscular dysplasia
128
Suspect what if unexplained HTN in woman < 40
Renal Artery Stenosis
129
pts with HTN and RAS MC have what other condition
>45 yrs with atherosclerotic disease hx
130
risk factors of renal artery stenosis
1. atherosclerotic disease
2. CKD
3. DM
4. tobacco use
5. HTN
131
s/s of RAS?
causes?
**HTN, abd bruit** (refractory or new-onset)
* Pulmonary edema with poorly controlled HTN
* AKI after starting an ACE inhibitor
132
lab findings for RAS
elevated BUN/Cr if significant ischemia
133
imaging needed/findings for RAS
| describe imaging options
US - asymmetric kidneys (if unilateral RAS) or small hyperechoic kidneys (if bilateral RAS)
* **Doppler US** - >90% sensitive and specific with good sonographer
- Very operator and pt dependent
- Poor choice - obese pt, interfering bowel gas, or if pt cannot lie supine
* CT angiography - may be less accurate, more expensive than US - Uses IV contrast
* MRA - excellent but expensive; uses contrast
**Renal angiography - gold standard**
134
what could lead to a false positive of RAS in imaging?
MRA
Turbulent blood flow = false + results
135
tx for RAS
medical management, surgery
* Angioplasty - can reduce number of anti-HTN meds; does not change progression of disease
* Surgical bypass - more risks and no superior efficacy to angioplasty
| intervention not proven better > meds for HTN, complications
## Footnote
Stenting produces better results than not
136
Hypertensive nephropathy
Sclerosis of arteries and arterioles
Interstitial fibrosis and decreased glomerular tuft
Nephrosclerosis
Up to 27% of ESRD pts have HTN as cause of CKD
137
risk factors for nephrosclerosis
* **African American race - 5x more common**
* Increased age, smoking, hypercholesterolemia
* Longstanding uncontrolled HTN
138
tx for nephroscleroisis
**management of HTN
**
Most pts require multiple antihypertensives
**Thiazide diuretics** and **ACE/ARB** MC
139
Emboli to kidneys → usually due to cholesterol
crystals breaking free of vascular plaque and lodging in downstream microvessels
Cholesterol Atheroembolic Disease
140
Cholesterol Atheroembolic Disease often follow ____
| the cause of it
angiographic procedures
May see with vascular surgery, trauma, heparin, thrombolytics
141
risk factors for Cholesterol Atheroembolic Disease
male, DM, HTN, ischemic cardiac disease
142
s/s of cholesterol atheroembolic disease
Onset usually 1-14 days after inciting event
* **worsening HTN and renal function**
* < 50% of pts have signs of embolic disease - fever, abdominal pain, wt loss
* **livedo reticularis, localized gangrene**
143
labs with increased Cr, eosinophilia (60-80%), elevated ESR, low complement
are with what dx
| CKD
Cholesterol Atheroembolic Disease
144
how to definitively dx of Cholesterol Atheroembolic Disease
kidney biopsy
145
tx for Cholesterol Atheroembolic Disease
no specific effective therapy
* **Statins**
* Steroids (controversial)
* Supportive tx
