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What Are The Risks Of Hip Replacement Before Beginning Kidney Treatment?
Question: I have membraneous nephropathy from primary causes and currently exhibiting symptoms of nephrotic syndrome. I was supposed to get a hip replacement, but the surgery was postponed due to the kidney issue. I currently have an antibiotic spacer in the hip, and have had this one since December (original was placed in November). What are the risks of getting the hip replacement before beginning kidney treatment, and is it recommended? I have postponed the treatment since the steroids and immunosuppressants will put me at more risk for infections in the event we go with the hip replacement first.
Brief Answer:
mgn with hip infection
Detailed Answer:
Hi,
You have not mentioned the amount or proteinuria per day, serum creatinine levels and amount of swelling you are having.
suppose your creatinine is stable. there is not much swelling or controlled on medication. then is is better to go for hip operation first. thought the healing may be slow but once healing is complete and there is no infection you can start immunosupression to control the nephrotic state.
If you do the other way around and start immunosupression, then you run the risk of having recurrence of infection in the joint space if the infection has not cleared completely.
Not all membranous nephritis need treatment with immunosupression. so that aspect also needs to be looked into depending on your kidney biopsy findings and present results of lab tests.
best wishes
mgn with hip infection
Detailed Answer:
Hi,
You have not mentioned the amount or proteinuria per day, serum creatinine levels and amount of swelling you are having.
suppose your creatinine is stable. there is not much swelling or controlled on medication. then is is better to go for hip operation first. thought the healing may be slow but once healing is complete and there is no infection you can start immunosupression to control the nephrotic state.
If you do the other way around and start immunosupression, then you run the risk of having recurrence of infection in the joint space if the infection has not cleared completely.
Not all membranous nephritis need treatment with immunosupression. so that aspect also needs to be looked into depending on your kidney biopsy findings and present results of lab tests.
best wishes
Above answer was peer-reviewed by :
Dr. Vinay Bhardwaj
Thank you for your quick response.
The following are my labs and the biopsy report, and my apologies for not including them previously.
Urine Protein: 7414 MG/TV in 24 hour collection
Urine Creatinine: 1230
Biopsy findings (pasting from pathologist's report)
LIGHT MICROSCOPY: The specimen is that of a portion renal
cortex and medulla, and its histologic sections are subjected to
hematoxylin & eosin, PAS, XXXXXXX and Masson trichrome staining procedures for morphologic evaluation.
In aggregate, about 27 glomeruli are included in the biopsy. One or two of the glomeruli are sclerosed or in the process of being sclerosed. None of them are segmentally hyalinosed. No foamy transformation of intrinsic cells is observed.
None of the intact glomeruli have ischemic-collapsed capillary network. The glomeruli in general are slightly enlarged, and almost all of them show minimal
hypercellularity related to proliferation of mesangial and endothelial cells, and minimal influx of PMNs/mononuclear cells. The endothelial cells are hypertrophic. Podocytes are prominent in several of the glomerular capillary loops.
The basement membranes of the capillary loops are slightly thickened, and mesangial matrices are minimally increased in some of the glomeruli, as assessed by PAS and XXXXXXX stain. None of the capillaries yield wire-loop appearance. None
of the glomeruli show lobular accentuation. Mesangial interposition with reduplication of basal lamina is not readily seen in any of the capillary
loops.
None of the glomeruli include suspicious hyaline thrombi in their capillary loops, and no fibrin thrombi are seen in any of the glomeruli. None of the glomeruli include fresh cellular crescents or adhesions with Bowman’s capsule.
None of the glomeruli include foci suspicious for karyorrhexis .
The tubules show moderate degenerative changes that are associated with minimal regenerative activity. Many of the tubules contain PAS-positive absorption droplets in their cytoplasm, while many others have undergone mild vacuolar degeneration. A minimal degree of tubular atrophy is observed. Two or three of the tubules contain hyaline/granular casts in their XXXXXXX
RBCs are not seen in the XXXXXXX of any of the tubules. The interstitium is minimally scarred, as revealed by Masson’s trichrome staining. No significant edema is present. The interstitium contains mild focal and scattered cellular infiltrates. The cellular infiltrates are made up of lymphocytes and a few monocytes and eosinophils. No foci with tubulitis are observed. No
foci of hemorrhage are seen. No foci of calcinosis are present. Overall, about 5% of the renal functional parenchyma is effaced due to tubular atrophy, interstitial fibrosis or cellular infiltrates. Several small blood vessels are included in the biopsy, and they show mild focal thickening of their walls. No foci suspicious for intimal arteritis are observed.
None of the small blood vessels contain any suspicious thrombi. A few of the arterioles are included and they are minimally thickened, and none of
them seems to have undergone hyalinosis. No foci suspicious for capillitis are observed.
IMMUNOFLUORESCENT MICROSCOPY: Please see the attached
report or in the Cerner.
ELECTRON MICROSCOPY: Two glomeruli are examined, and the following ultrastructural alterations are observed. The cellular changes include diffuse fusion of the foot processes of the podocytes associated with cytoskeletal
changes and villous transformation. The podocytes show mild to moderate focal increase of phogolysomes/phagosomes in their cytoplasm. The endothelial cells show moderate degree of hypertrophy. The mesangial cells have undergone minimal focal hyperplasia. A minimal capillary influx of inflammatory cells (monocytes/PMNs) is seen. Tubulo-reticular inclusions (TRI) are not seen in
glomerular or extra-glomerular endothelia. The ECM changes include a mild focal expansion of the mesangial regions. The GBMs seem to be slightly thickened, and are not wrinkled at any place. No capillary loops with mesangial interposition are
seen. Mild to moderate focal expansion of the subendothelial spaces is seen. Many well-defined electron-dense deposits are present in subepithelial regions of the glomerulus. Some of these deposits resemble subepithelial humps and at times they are confluent. No deposits with fibrillary material are present.
IMMUNOFLUORESCENCE STUDIES (KIDNEY)
Anti-IgG (++++) Glomerular capillary wall reactivity
Anti-IgA (++) Glomerular capillary wall reactivity
Anti-IgM No significant-specific reactivity
Anti-C1q No significant-specific reactivity
Anti-C3 (+++) Glomerular capillary wall reactivity
Anti-Fibrinogen No significant-specific reactivity
Anti-albumin (++) Focal tubular epithelial reactivity
Anti-kappa (+++) Glomerular capillary wall reactivity
Anti-lambda (+++) Glomerular capillary wall reactivity
Negative control Negative
Comment:
Three Glomeruli present
This test was developed and its performance characteristics determined by Northwestern Memorial Hospital Immunohistochemistry Laboratory. It has not been cleared or approved by the U.S. Food and Drug Administration. The FDA has determined that such clearance or approval is not necessary. This test is used for clinical purposes. It should not be regarded as investigational or for research. This laboratory is certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA-88) as qualified to perform high complexity clinical laboratory testing.
Specimen/Gross Description
A. Received in formalin labeled with the patient's name and designated on the requisition as "native kidney biopsy," are two cores of soft pink-tan tissue measuring 0.9 cm and 1.4 cm in length and both measuring 0.1 cm in diameter. The entire specimen is submitted in cassette A1.
The following are my labs and the biopsy report, and my apologies for not including them previously.
Urine Protein: 7414 MG/TV in 24 hour collection
Urine Creatinine: 1230
Biopsy findings (pasting from pathologist's report)
LIGHT MICROSCOPY: The specimen is that of a portion renal
cortex and medulla, and its histologic sections are subjected to
hematoxylin & eosin, PAS, XXXXXXX and Masson trichrome staining procedures for morphologic evaluation.
In aggregate, about 27 glomeruli are included in the biopsy. One or two of the glomeruli are sclerosed or in the process of being sclerosed. None of them are segmentally hyalinosed. No foamy transformation of intrinsic cells is observed.
None of the intact glomeruli have ischemic-collapsed capillary network. The glomeruli in general are slightly enlarged, and almost all of them show minimal
hypercellularity related to proliferation of mesangial and endothelial cells, and minimal influx of PMNs/mononuclear cells. The endothelial cells are hypertrophic. Podocytes are prominent in several of the glomerular capillary loops.
The basement membranes of the capillary loops are slightly thickened, and mesangial matrices are minimally increased in some of the glomeruli, as assessed by PAS and XXXXXXX stain. None of the capillaries yield wire-loop appearance. None
of the glomeruli show lobular accentuation. Mesangial interposition with reduplication of basal lamina is not readily seen in any of the capillary
loops.
None of the glomeruli include suspicious hyaline thrombi in their capillary loops, and no fibrin thrombi are seen in any of the glomeruli. None of the glomeruli include fresh cellular crescents or adhesions with Bowman’s capsule.
None of the glomeruli include foci suspicious for karyorrhexis .
The tubules show moderate degenerative changes that are associated with minimal regenerative activity. Many of the tubules contain PAS-positive absorption droplets in their cytoplasm, while many others have undergone mild vacuolar degeneration. A minimal degree of tubular atrophy is observed. Two or three of the tubules contain hyaline/granular casts in their XXXXXXX
RBCs are not seen in the XXXXXXX of any of the tubules. The interstitium is minimally scarred, as revealed by Masson’s trichrome staining. No significant edema is present. The interstitium contains mild focal and scattered cellular infiltrates. The cellular infiltrates are made up of lymphocytes and a few monocytes and eosinophils. No foci with tubulitis are observed. No
foci of hemorrhage are seen. No foci of calcinosis are present. Overall, about 5% of the renal functional parenchyma is effaced due to tubular atrophy, interstitial fibrosis or cellular infiltrates. Several small blood vessels are included in the biopsy, and they show mild focal thickening of their walls. No foci suspicious for intimal arteritis are observed.
None of the small blood vessels contain any suspicious thrombi. A few of the arterioles are included and they are minimally thickened, and none of
them seems to have undergone hyalinosis. No foci suspicious for capillitis are observed.
IMMUNOFLUORESCENT MICROSCOPY: Please see the attached
report or in the Cerner.
ELECTRON MICROSCOPY: Two glomeruli are examined, and the following ultrastructural alterations are observed. The cellular changes include diffuse fusion of the foot processes of the podocytes associated with cytoskeletal
changes and villous transformation. The podocytes show mild to moderate focal increase of phogolysomes/phagosomes in their cytoplasm. The endothelial cells show moderate degree of hypertrophy. The mesangial cells have undergone minimal focal hyperplasia. A minimal capillary influx of inflammatory cells (monocytes/PMNs) is seen. Tubulo-reticular inclusions (TRI) are not seen in
glomerular or extra-glomerular endothelia. The ECM changes include a mild focal expansion of the mesangial regions. The GBMs seem to be slightly thickened, and are not wrinkled at any place. No capillary loops with mesangial interposition are
seen. Mild to moderate focal expansion of the subendothelial spaces is seen. Many well-defined electron-dense deposits are present in subepithelial regions of the glomerulus. Some of these deposits resemble subepithelial humps and at times they are confluent. No deposits with fibrillary material are present.
IMMUNOFLUORESCENCE STUDIES (KIDNEY)
Anti-IgG (++++) Glomerular capillary wall reactivity
Anti-IgA (++) Glomerular capillary wall reactivity
Anti-IgM No significant-specific reactivity
Anti-C1q No significant-specific reactivity
Anti-C3 (+++) Glomerular capillary wall reactivity
Anti-Fibrinogen No significant-specific reactivity
Anti-albumin (++) Focal tubular epithelial reactivity
Anti-kappa (+++) Glomerular capillary wall reactivity
Anti-lambda (+++) Glomerular capillary wall reactivity
Negative control Negative
Comment:
Three Glomeruli present
This test was developed and its performance characteristics determined by Northwestern Memorial Hospital Immunohistochemistry Laboratory. It has not been cleared or approved by the U.S. Food and Drug Administration. The FDA has determined that such clearance or approval is not necessary. This test is used for clinical purposes. It should not be regarded as investigational or for research. This laboratory is certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA-88) as qualified to perform high complexity clinical laboratory testing.
Specimen/Gross Description
A. Received in formalin labeled with the patient's name and designated on the requisition as "native kidney biopsy," are two cores of soft pink-tan tissue measuring 0.9 cm and 1.4 cm in length and both measuring 0.1 cm in diameter. The entire specimen is submitted in cassette A1.
Based on the above info, my creatinine levels are stable (and have been for two different tests), but my proteinuria is quite high. The swelling is well controlled via diuretics and use of compression stockings. I do not have high blood pressure either.
PT/INR also show clotting within range (PT: 10.6; INR: 1.0)
An ultrasound showed the kidneys look normal.
Based on this additional info, would your initial response be the same? Thanks for your help.
PT/INR also show clotting within range (PT: 10.6; INR: 1.0)
An ultrasound showed the kidneys look normal.
Based on this additional info, would your initial response be the same? Thanks for your help.
Brief Answer:
MGN and joint replacement
Detailed Answer:
Hi,
I have gone through your reports. The disease seems to be active and may not resolve spontaneously. You will need immunosupressive agents like cyclophosphamide, mycophenolate or tacrolimus along with low dose steroid. if we have to go for this we have to be sure that you do not have any infection. if your orthopedics doctor feels that there is no infection at all now then you may start these. But if in doubt these medicines should not be started.
But i doubt if your orthopedics will be able to comment on that and in that case only option is to go for hip surgery first , but then here problem is delayed healing. I think still it may be a good option.
Best wishes
MGN and joint replacement
Detailed Answer:
Hi,
I have gone through your reports. The disease seems to be active and may not resolve spontaneously. You will need immunosupressive agents like cyclophosphamide, mycophenolate or tacrolimus along with low dose steroid. if we have to go for this we have to be sure that you do not have any infection. if your orthopedics doctor feels that there is no infection at all now then you may start these. But if in doubt these medicines should not be started.
But i doubt if your orthopedics will be able to comment on that and in that case only option is to go for hip surgery first , but then here problem is delayed healing. I think still it may be a good option.
Best wishes
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Hi Doctor, again thanks for your quick reply.
There is no infection - no visible signs, and my CRP test shows normal range. The sedimentation rate is high, but that is due to the kidney disease. I have been monitored on a regular basis by infectious diseases specialists due to my past infections.
The concern is whether to proceed with the surgery first or to start the immunosuppressants. The immunosuppressant the nephrologist has recommended is cyclosporin. This was going to be the immediate treatment, and then waiting a few months before starting steroids. However, the orthopedic surgeons on my case told me not to start immunosuppressants as surgery first may be the better option.
I am confused with what the better choice is - have surgery now or later. Now would imply, as you suggested, a slower healing process. But delaying, we will not know how long until I could have the surgery as it would depend on me recovering from the immunosuppressants. This would leave me in my current state of very poor quality of life, increasing pain, lack of mobility, etc. I would also be at higher risk of contracting infection due to the immunosuppressed state.
Again, thanks for your thoughts. I am just confused as to what the better treatment is given my current state.
There is no infection - no visible signs, and my CRP test shows normal range. The sedimentation rate is high, but that is due to the kidney disease. I have been monitored on a regular basis by infectious diseases specialists due to my past infections.
The concern is whether to proceed with the surgery first or to start the immunosuppressants. The immunosuppressant the nephrologist has recommended is cyclosporin. This was going to be the immediate treatment, and then waiting a few months before starting steroids. However, the orthopedic surgeons on my case told me not to start immunosuppressants as surgery first may be the better option.
I am confused with what the better choice is - have surgery now or later. Now would imply, as you suggested, a slower healing process. But delaying, we will not know how long until I could have the surgery as it would depend on me recovering from the immunosuppressants. This would leave me in my current state of very poor quality of life, increasing pain, lack of mobility, etc. I would also be at higher risk of contracting infection due to the immunosuppressed state.
Again, thanks for your thoughts. I am just confused as to what the better treatment is given my current state.
Answered by
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