Bookmark & Share
Connect With Us
- Acute Kidney Injury
- Alport Syndrome
- Ask the Doctor
- AV Fistula
- Birth Defects/Urinary Tract Abnormalities
- BK virus
- Blood/Urine Testing For Kidney Disease
- Chronic Kidney Disease
- Clinical Trials/Studies
- End of Life Issues
- Goodpasture's Symdrome
- Herbal Supplements in Kidney Disease/Failure
- Hydronephrosis and Hydroureter
- Hypertension/High Blood Pressure
- IgA Nephropathy/IgA Dominant Glomerulonephritis
- Insurance & Medicare Coverage
- Kidney Biopsy
- Kidney Cancer
- Kidney Cysts
- Kidney Failure
- Kidney Mass
- Kidney Stones
- Kidney-Related Health Questions
- Laboratory Testing
- Living Donation
- Medication and Kidney Disease
- Medication and Kidney Function
- Medullary Sponge Kidney
- Minimal Change Disease
- Nephrectomy / One kidney
- Nephrotic Syndrome
- organ donation
- Pediatric Issues
- Polycystic Kidney Disease
- Pregnancy / Kids
- Risk factors
- Serum Creatinine
- Sexual health
- Symptoms and Side Effects
- Urinary Tract Infection/Pyelonephritis
- Urological Issues
Category Archives: Gout
Hi- History: 60 y.o female Dx’d with Crohn’s 2010. Put on Mesalamine. Developed Interstitial nephrites dx’d in 2011. Taken off Mesalamine upon which I went into Crohn’s remission for 2 years. My Creatinine which was up to 1.2 returned to .89. In 2013 Crohn’s returned. I was being treated with Infliximab for Crohn’s and then after the 13th infusion noticed an ammonia taste in my mouth. That was the only symptom. A renal panel drawn prior to the next infusion revealed a Creat. over 3 and GFR of 15, I’d like to know whether you think the following biopsy points to Crohn’s as the cause or Infliximab as the cause of this renal injury. Also, was I more likely to have interstitial nephritis again since I had it previously? Thanks. KIDNEY BIOPSY (NEEDLE) SEVERE ACUTE AND CHRONIC INTERSTITIAL NEPHRITIS, WITH AN ISOLATED NON-NECROTIZING GRANULOMA (SEE NOTE) NO EVIDENCE OF IMMUNE COMPLEX-MEDIATED OR PARAPROTEIN DEPOSITION DISEASE; CRITERIA FOR IgG4 RELATED DISEASE ARE NOT MET IN THIS SAMPLE MODERATE CHRONIC CHANGES OF THE PARENCHYMA, INCLUDING: – GLOBAL GLOMERULOSCLEROSIS (10% OF GLOMERULI) – MODERATE TUBULAR ATROPHY AND INTERSTITIAL FIBROSIS – SEVERE ARTERIAL AND ARTERIOLAR SCLEROSIS NOTE: The biopsy reveals widespread plasma cell-rich interstitial inflammation, with a focal small non-necrotizing granuloma. This type of injury is most commonly related to a hypersensitivity reaction to drugs (sulfonamides, beta-lactam and other antibiotics, anti-viral agents, diuretics, NSAIDs, cimetidine and H2-blockers, and a long list of miscellaneous drugs). Other causes of chronic active interstitial nephritis include severe various infectious processes, metabolic diseases (gout and hyperuricemic conditions), toxic processes (lithium, lead, and other heavy metals), aristolochic acid nephropathy (Chinese herb nephropathy), physical causes (obstruction and radiation injury), and other conditions (Balkan nephropathy, sarcoidosis, “idiopathic” interstitial nephritis). For most of these conditions there are no specific or even characteristic morphological findings, and the disease process can only be diagnosed by correlating the biopsy findings and the history of the use or exposure to certain drugs or substances. There is no evidence of immune complex or paraprotein deposition. IgG4 related disease is unlikely, given the results of immunohistochemistry studies (see results below). MICROSCOPIC DESCRIPTION: Sections of formalin-fixed, paraffin embedded tissue were evaluated using H&E, PAS, JMS, and trichrome stains. An H&E-stained frozen section taken from the tissue allocated for immunofluorescence microscopy and semi-thin toluidine blue-stained epoxy sections of the tissue processed for electron microscopy were also evaluated using light microscopy. The sample consists of 57 glomeruli (LM-48; IF-5; EM-4), of which 6 are globally sclerosed and several glomeruli appear hypoperfused. The non-sclerosed glomeruli are of normal size and reveal normal thickness of the glomerular capillary loops. Significant endocapillary proliferation or cellular crescents are not seen in the glomeruli. The mesangium is not significantly expanded. The interstitium reveals large areas of intense inflammation, associated with mild edema and focal tubulitis. The infiltrates are composed of lymphocytes and many plasma cells, several eosinophils and scattered neutrophils. Isolated foci of Tamm-Horsfall protein inspissation are present in the interstitium. A focal small non-necrotizing granuloma is noted, with epithelioid cells, lymphocytes, and an isolated multinucleated giant cell. In less involved areas, tubules reveal normal cellular details. In inflamed areas, tubules reveal tubulitis and focal degenerative changes. Several tubules also contain necrotic cellular debris. Several PAS-positive hyaline casts are also noted. The sample shows moderate tubular atrophy and interstitial fibrosis. Arteries and arterioles show severe sclerosis. Arterioles also show focal hyaline degeneration. IMMUNOHISTOCHEMISTRY RESULTS: The staining for CD138, IgG4, and IgG were performed using immunoperoxidase technique. Numerous CD138-positive plasma cells were identified, but only isolated cells stain for IgG4. The positive control slide and the patient’s negative non-immune control slide (normal serum) show appropriate reactivity. The immunohistochemical tests performed at Brigham and Women’s Hospital were developed and their performance characteristics determined by the Immunohistochemistry Laboratories in the Department of Pathology at BWH. They have not been cleared or approved by the U.S. Food and Drug Administration (FDA). The FDA has determined that such clearance or approval is not necessary. IMMUNOFLUORESCENCE MICROSCOPY: KIDNEY BIOPSY #: E15-926 The sections of the sample submitted for immunofluorescence studies were incubated with antibodies specific for the heavy chains of IgG, IgA, and IgM, for kappa and lambda light chains, fibrin, albumin, and complement components C3 and C1q. The sample contains 5 glomeruli. There is 1 globally sclerosed glomerulus. No significant immune deposits are seen in the glomeruli. IgM stain shows dusty reactivity in the background of the tissue; there is also fine granular reactivity for IgM (trace) along the glomerular capillary loops. Dull reactivity with fibrin is noted along the glomerular capillary loops. Tubular basement membranes show focal fine granular deposition of C3 (trace). Tubules contain several intraluminal casts reactive for polyclonal IgA. The interstitium reveals scattered fibrin deposits. Some interstitial inflammatory cells are positive for kappa or lambda light chains. The vessels exhibit focal deposition of C3. There is no difference in reactivity between kappa and lambda light chains in the glomeruli, tubular casts or background of the tissue. The immunofluorescence microscopy tests performed at Brigham and Women’s Hospital were developed and their performance characteristics determined by the Immunohistochemistry Laboratories in the Department of Pathology at BWH. They have not been cleared or approved by the U.S. Food and Drug Administration (FDA). The FDA has determined that such clearance or approval is not necessary. ELECTRON MICROSCOPY: KIDNEY BIOPSY #: E15-926 Blocks: 1 Block examined: 1 thick section; 1 thin section. The sample submitted for electron microscopy examination contains 3 glomeruli; 2 glomeruli are examined ultrastructurally. The glomerular visceral epithelial cells reveal moderate effacement of their foot processes. The glomerular basement membranes are segmentally attenuated. Morphometric analysis was performed on 105 sites, using orthogonal intercept method. The harmonic mean of the glomerular basement membrane thickness is 274 nm. The subendothelial space of the basement membrane is segmentally expanded by electron-lucent fluffy material in a few capillaries; a new layer of basement membrane material is formed under the displaced endothelium (double contours). The endothelial cells show no significant changes. The mesangium reveals normal cellular elements and a normal amount of matrix. No electron dense deposits are present in the mesangium. CLINICAL DATA: History: A 60-year-old female with Crohn’s disease who presents with AKI. BUN 44, Cr 2.79 (baseline 0.89 in 2/2014; peak 3.24 on 7/18/15), Alb 4.0, HbA1c 5.4, C3 86, C4 15, free kappa LC/lambda LC ratio 2.45, negative hepatitis B/C, negative SPEP, urine sediment WBC 4/hpf, UA blood negative, proteinuria 0.14 g/gCr. TISSUE SUBMITTED: A/1. LM. B/2. IF. C/3. EM.
I am not able to give a medical opinion without performing a complete history and physical examination. I suggest that you discuss your concerns with your nephrologist. The biopsy diagnosis appears to be an interstitial nephritis but I’m not sure … Continue reading →
My husband is 40 years old and he has creatine level 1.5. Will there be any kidney problem? He has RA and Gout.
I am unable to make a specific diagnosis based on the information that you present. In order to make a diagnosis of chronic kidney disease (CKD) your husband must have both blood and urine testing. I suggest you consult with … Continue reading →
Gout is very common in chronic kidney disease (CKD). CKD can cause gout and gout can cause CKD. If you have recurring attacks of gout you should see your physician and be tested for CKD.
I get kidney stones on a regular basis that pass on there own. I seem to have pain in my foot associated with the stones, almost like a burning sensation. Is this normal or could it be caused by something else?
I do not know why you should experience foot pain associated with kidney stones. This does not make sense. Patients with gout may get painful joints and also kidney stones that come from gout stones. I can not explain the … Continue reading →
About 10 years ago my ex-husband, who has always been in good health, developed hematuria. There was no work up then. About 3 years ago, he developed multiple kidney stones in only the left kidney. He has also experienced multiple episodes of gout. His left kidney has atrophied to 6mm transverse x 8mm AP x 9mm sup-inf-inf. He is on Potassium Citrate 3x daily with Allopurinol. He had shock wave lithotripsy 08/16 with questionable results. A renal US in 11/16 noted again multiple kidneys stones with further atrophy. He has had several more gout attacks with this regime. GFR is 41. I am concerned about damage to kidney from persistent good sized stones. Should they be removed? Would a biopsy be warranted? Why are there stones in only the one kidney? Could it progress to involve the other? There is no family history of kidney disease or gout. Thank you for your help.
The problem that you raise is a urological problem and should be dealt with by a urologist. I am a nephrologist and have no experience with lithotripsy or surgery. I suggest that your ex-husband consult with a urologist and determine … Continue reading →
I have been taking 300 mg of Allopurinol for 32 years now. Any long term side effects? Over this time my creatinine value has gone up to 2.85. Who could I talk to about taking it for this long?
Allopurinol is a medication used to prevent acute attacks of gout and prevent joint damage from gout. It will also prevent gout kidney stones from forming. If you are tolerating the medication without side effects, then you should continue to … Continue reading →
I took allopurinol after chemotherapy to prevent gout and lower uric acid. High uric acid causes blood in my urine. and once uric acid level was back in range without blood in urine, the allopurinol started giving me constipation. I found when I didn’t take allopurinol, I wasn’t constipated. When I did take allopurinol, I was constipated again. The constipation puts a tremendous amount of stress on my lower back and spine. Something in the allopurinol makes me constipated. Do I discontinue allopurinol?
In this case, I suggest that you discuss the side effects of allopurinol with your physician. There are other alternatives to taking allopurinol. There is a drug called febuxostat (Brand name Ulrich) that can be used to treat gout and … Continue reading →
This is a problem of the chicken or the egg. An elevated blood uric acid level can be associated with acute and chronic gouty arthritis. An elevated blood uric acid level over many years can also be associated with kidney … Continue reading →
Allopurinol is a medication used to treat gout. The dose of allopurinol should be sufficient to lower the blood uric acid level so as to prevent attacks of gout. In general, the goal is to get the blood uric acid … Continue reading →
Can taking a 10 MG daily tablet of the Ace Inhibitor Lotensen (Benazepril) help slow down the decline in kidney function for someone in the early stages of chronic kidney disease?
Angiotensin Converting Enzyme (ACE) inhibitors such as Benazepril have been shown to slow the progression of chronic kidney disease (CKD) especially in those patients who have excess protein in their urine. I do recommend such treatment frequently. For more information … Continue reading →