Category Archives: Kidney Biopsy

I have proteinuria for over 9 years. It was first detected in 2008. I’m a male person, 36 years old, with 183 cm height and 90 kg weight. My blood pressure is 120/80 most often. My results from the lab August -03 2017 AlkP 66 U/L AST 16 U/L ALT 16 U/L Gluc C 4.77 mmol/L Urea 4.5 mmol/L CreaC 80.30 umol/L UA 361.8 umol/L TP 72 g/L AlbG 47 g/L Gllob. 25 g/L Na-C 139 mmol/L K-C 4.8 mmol/L CaC 2.39 mmol/L Phos 0.95 mmol/L IgA 2.38 g/L IgG 10.70 g/L IgM 0.62 g/L C3 1.1 g/L C4 0.2 g/L Trig 0.7 mmol/L Clol 5.1 mmol/L UHDL 1.22 mmol/L LDL CALC 3.5 Upro 0.69 g/L (proteins in 24 hour urine) I also did tests during the last few months. (the results were 0.39 , 0.60 , 0.62 g/L) My doctor advised me to do a Biopsy in order to detect the reason of kidney damage. What do you think about my lab results? Is it allowed for me to do physical exercises with this condition ( for example 1 hour of bicycling, or 2 hours of walking 5-6 times per week), knowing that this will increase the amount of proteins in my urine аdditionally? This is very important for me because my BMI is over 26 and I have overweight. I want to do exercise so that I can have a normal weight. Do these proteins that are passing from the kidneys to the urine are damaging my kidneys?

I am unable to make a specific diagnosis of kidney disease based on the information that you present.  You have excess protein in your urine and this can both cause kidney disease and also be the result of kidney disease. … Continue reading

Posted in Ask the Doctor, Chronic Kidney Disease, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Symptoms and Side Effects, Treatments

Hello, My fathers kidneys have been declining since 1997 To make a long story short his PCP failed him by not referring him to Nephrologist (based on lab results) He had a complete workout w/ his specialist only to say his kidney functions were at 40% bloodwork, imaging showed no cause as to why his kidneys were declining in function. He recently July 18, 2017 switched to another specialist , the Dr ran extensive work up consisting of blood, lab, imaging tests as well as had his earlier medical records and tests. The dr said he had chronic kidney disease stage 4 All tests revealed indicating declines in both kidneys, Scarring on both kidneys. Sorry I’m not more precise as I’m getting info from my mother. I am going to request his lab results for myself. The Dr said he could not find a cause to what is causing his chronic kidney disease. My dad always had low blood pressure, no diabetes, was not overweight, led active lifestyle, no cardiac issues. No medical history that would explain. He served in Vietnam was drafted late 1960’s. He did receive 3 Purple Hearts. I do know he fell on landmine to save someone in his troop and had graphs put on his face. Also the use of agent Orange. I don’t believe (unsure) if Dr tested for genetic Markers, chromosomal etc.. he did have a biopsy years back which did not help or aid in explaining a cause. My question is what could be causing this? Is their a test that’s not standard or well known to do to help in finding a cause? I know environment, genetics and congenital could be possible causes. I am unsure if blood tests done or workup would show this. Any help would be appreciated. I am requesting my dads medical record. He is 73, Italian (born in Bari, Italy) has lived in MA area since he migrated here. He always had low blood pressure, his kidneys have high blood pressure, protein in urine . The ultrasound revealed small kidneys with extensive scarring. Hope this helps. I apologize for not being more specific while writing this. Any information or resources would be greatly appreciated.

A kidney biopsy should be definitive as far as indicating the cause of chronic kidney disease (CKD).  The kidney biopsy, if the tissue sample was adequate, should give the pathological cause of the CKD.  I suggest that you review the … Continue reading

Posted in Ask the Doctor, Blood/Urine Testing For Kidney Disease, Chronic Kidney Disease, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Nephrologist, Symptoms and Side Effects, Treatments

Hello sir, Patient’s name is ********. Her Histopathological report: Renal biopsy (5slides for opinion) shows 21 glomeruli, 16 show near global glomerulosclerosis. Remaining shows mild increase in mesangial cellularity, capillary wall thickening with double contouring, endothelial swelling, narrowing and occlusion of capillary lumina(acellular glomeruli). There is segmental fibrin disposition and three fibrocellular crescents are also noted. There is modular tubular atrophy. Histological features favour thrombotic microangiopathy with 70-80% chronicity in all renal compartments. Doctors have suggested Plasma therapy now. The patient had dialysis 5-6 times. Today first session of plasma was administered. It is to be given for 15 days daily to replace the plasma. (Maybe, technically, I am wrong about just the plasma thing) I will be extremely grateful if you could advise the expected course of treatment. I will be online after 23 Hrs. I am from India.

I am unable to make medical recommendations, treatment recommendations or offer a prognosis without performing a complete history and physical examination.  The kidney biopsy suggest that the patient could have Hemolytic Uremic Syndrome (HUS), Thombotic Thrombocytopenic Purpura (TTP), malignant hypertension, … Continue reading

Posted in Ask the Doctor, Blood/Urine Testing For Kidney Disease, Chronic Kidney Disease, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Medication and Kidney Disease, Symptoms and Side Effects, Treatments

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

Posted in Ask the Doctor, Blood/Urine Testing For Kidney Disease, Chronic Kidney Disease, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Symptoms and Side Effects, Treatments

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

Posted in Ask the Doctor, Chronic Kidney Disease, GFR, Gout, Herbal Supplements in Kidney Disease/Failure, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Nephrologist, Symptoms and Side Effects, Treatments

Hello Dr. Spry, I was diagnosed with FSGS in 2014 after a routine labwork showed diminished kidney function. Creatinine levels have remain between 2.1 – 2.4 for the past 2 yrs, with kidney function between 35 – 40. Currently taking BP medications with avg reading of ~135/88. My only other ailment is my cholesterol being high, but so far I have not been able to tolerate the statin medication my doctors have provided me. I’m 37 yrs old and need to know what happens next? What steps can I take to prevent kidney failure? Is there any new health technologies that provide alternative treatment for my condition? Thanks.

Currently, the recommended treatment for focal segmental glomerulosclerosis  (FSGS) is based on the kidney biopsy and subtype of the disease.  In most cases, the basic treatment is to use ACE-inhibitors or ARB agents to treat and control blood pressure.  The … Continue reading

Posted in Ask the Doctor, Blood/Urine Testing For Kidney Disease, Chronic Kidney Disease, Diet/Nutrition, FSGS, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Nephrologist, Treatments

Dear Doctor, Please see the below recent lab reports for your reference. (Done on 24/06/2017) Urine microalbumin: 983 mg/dl, urine microalbumin/creatine ratio: 1262 mg/dl, Albumin:4.62, creatinine: 1.44, BUN:15.6, Total cholesterol: 275, Uric acid: 8. I have been taking Olmesarten 20 mg for 2 yrs for blood pressure. Then the nephrologist changed this tablet to Lercadip 20 mg, but after taking lercadip, I feel palpitation so again changed to Tab Micardis 40 mg. I have started taking Tab Micardis from last week only. Now the doctor advised me to go for renal biopsy. I am working in Dubai.

I am unable to make a specific diagnosis based on the information that you present.  You have kidney disease based on the increase in urine protein (microalbumin) but I cannot make any other diagnosis.  A kidney biopsy would clearly show … Continue reading

Posted in Ask the Doctor, Blood/Urine Testing For Kidney Disease, Chronic Kidney Disease, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Microalbuminuria, Symptoms and Side Effects, Treatments

Hi, I had edema and some pain in my foot. I applied to hospital. According to my lab results everything was okay (including creatinin 0.98) except protein amount urine (3256 mg / 2.2 Litre). They made biopsy and the result was fsgs (collapsing). My BMI is over 32 (183 cm 110 kg and my blood tension was 16 – 10. Doctor gave me Delix 5 mg (1 per day) and poor protein diet. Is that mean “My kidney disease is because of obesity and tension?” If yes, can it be reversed?

Focal segmental glomerulosclerosis (FSGS) has many different causes, including obesity.  High blood pressure can be seen in patients with FSGS but does not normally cause FSGS.  I am unable to make a specific diagnosis without performing a complete history and … Continue reading

Posted in Ask the Doctor, Blood/Urine Testing For Kidney Disease, Chronic Kidney Disease, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Living Donation, Treatments

I am male, 30 years old and I have Proteinuria. Doctors suspect some kind of Glomerulonephritis. One doctor thinks is IgA Nephropathy. And I am really confused and worried. I decided to do a biopsy to find out in about a month from now. The laboratory results are confusing me a bit as they use different measurements. All are urine test results here. January 2017: Urinary Micro Albumin: 1132 mg/L Urinary Creatinine: 1.25 gm/L Albumin Creatinine Ratio (ACR) 905.0 mg/gm February 2017: Urinary Micro Albumin: 590 mg/L Urinary Creatinine: 0.60 gm/L Albumin Creatinine Ratio (ACR) 983.0 mg/gm May 2017: Urinary Albumin: 109.2 mg/dL Urinary Creatinine: 0.08 g/dL Albumin Creatinine Ratio (ACR) 1365 mg/g (Different laboratoy than the 2 previous) I will appreciate a lot if you kindly would give me your feedback.

The only result that you quote consistently is the urinary albumin to creatinine ratios.  The other results reflect the concentration of the urine and are not significant.  The urinary albumin to creatinine ratios are between 905 and 1365.  These numbers … Continue reading

Posted in Ask the Doctor, Chronic Kidney Disease, Hydronephrosis and Hydroureter, IgA Nephropathy/IgA Dominant Glomerulonephritis, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Nephrologist

I am a 51 y.o. caucasian woman with a GFR of 45, Creatinine of 1.27, 4.3 Albumin and BUN of 11. I am overweight, have slightly elevated cholesterol (204) though I exercise religiously 3x a week – 180 minutes total – doing cardio exercise, circuit training, and weight lifting. My BP is pretty average and I am not diabetic. My question is this: Am I at a point that I should pursue treatment with a nephrologist, or is it still relatively early? My GFR has dropped steadily for years and this is the highest creatinine reading I’ve had as well, so I am concerned.

The information that you provide would suggest that you have Stage 3 chronic kidney disease (CKD).  Most primary care physicians (PCP’s) are very capable of managing Stage 3 CKD.  The main treatment for your disease is likely to lose weight, … Continue reading

Posted in Ask the Doctor, Blood/Urine Testing For Kidney Disease, Chronic Kidney Disease, GFR, Hypertension/High Blood Pressure, Kidney Biopsy, Kidney-Related Health Questions, Laboratory Testing, Nephrologist, Treatments