CASES
An unusual case of Hyperkalemia
An unusual case of Hyperkalemia
Case 2
Mercury induced Kidney and Nerve disease.
( Do Not Consider anything Herbal/Ayurvedic is free of Side effects)
36 year old male, software engineer , was referred to me for Nephrotic syndrome( heavy protien leak in urine >3gm per day) in Oct 2018. He had swelling in both feet for 2 months. He also complained of unsteadiness of gait and weakness in both legs with difficulty in holding chappals and
squatting,upsquatting and climbing stairs.
When we looked at his 24 hour Urine protein- it was 12 gm .( normal is 150mg)
Clearly on examination patient had features of Nephrotic syndrome and Neuropathy.
A serological workup and Kidney biopsy was performed, which suggested a diagnosis of Minimal Change disease.
Neurologist was consulted for the weakness in limbs, on Nerve conduction study it was confirmed to be a demyelinating Neuropathy(GBS).
To rule out secondary causes for his kidney and Nerve disease, when we enquired in detail about the onset and course of illness,he mentioned that he was having a chronic back ache due to prolong
sitting as a software professional.For this he decided to go for Ayurvedic treatment at a very reputed institute in Dubai. He started the Ayurvedic treatment which consisted of 10 days whole body
massage and some Medicines which were prepared by the institute. One month later he started to get ulcers in mouth over tongue, and also bodyaches worsened. For next 6 weeks he kept on consulting ENT specialist and different doctors for the ulcers and body aches and had no much relief.
By then he had stopped taking the ayurvedic treatment as advised by an ENT surgeon. Almost a month later he noted swelling in feet and was diagnosed with Nephrotic syndrome.
Now we contacted the Ayurvedic professional who had prescribed him the medication for back pain, he confirmed the presence of Mercury and Gold in the medicine.
We then sent Electron Microscopy of the Kidney biopsy for confirmation of the histological diagnosis and meanwhile Steroids were started as treatment for Minimal Change disease.
For the Nerve conduction defect he was treated with IV Immunoglobulins, with which over 3-4 weeks he had improvement in the power of his legs, he was able to walk without support and imbalance had resolved.
Electron microscopy report that came after 2weeks changed our histological diagnosis to Membranous Nephropathy.
Now, Membranous Nephropathy can be a primary one, with auto immune cause or secondary to variety of causes one of them is also heavy metal induced especially Gold, Mercury etc.
To confirm the cause, we did ImmunoHistochemistry of the kidney biopsy, to look for Anti-PLA2 R antibody deposits , it was Negative.Blood Anti-PLA2 R levels were also negative.
This suggested that this Membranous Nephropathy was secondary , and to confirm the cause we did a 24 hour urine and blood Mercury level. The blood Mercury level was 21.93 mcg/L (Normal range-0.4- 7.5mcg/L).24 Hour Urinary Mercury level was 196.63mcg/day(Toxic range- above 50mcg/day)
This established the culprit was the Mercury in the Ayurvedic/Siddha Medicine which was used for backache, which caused this Kidney and Nerve damage.
Mercury Chelation Therapy:
He was then started on Succimer(DMSA) at 10mg/kg/dose every 8 hours for 5 days followed by 10mg/kg/dose every 12 hours for 14 days.
The 24 hour Urinary mercury levels decreased after the therapy was completed , but patient continued to have heavy proteinuria till now, the serum creatinine level is normal.
We expect recovery over 9 months , but it could also be a permanent damage.
Thus, any Ayurvedic / Siddha medicine containing heavy metals,like Gold,Silver,Arsenic,Lead,Mercury, should not be taken casually, or with the belief that all that is Ayurvedic is free of side effects.
Case 2
A Rare case of Gordon Syndrome
A 28 year old female , IT Professional, was referred to my Nephrology Clinic for evaluation of High Potassium levels in her blood.
This high potassium level was detected on a routine blood check up as part of her annual health check. She had no symptoms or any disease.
The primary physician who saw her gave her medication for getting the potassium down,and suggested dietary potassium restriction and saw after 2 weeks , still the potassium level was 6. Then he referred her to me for evaluation for this abnormally high potassium level.
She had no symptoms or signs of any disease. No h/o NSAID’S/ ACE- inhibitors/ARB's/MRA/AYURVEDIC/alternative medicines.No h/o arthritis, rash, alopecia,oral ulcers, photosensitivity, dryness of eyes, Raynauds phenomenon. No h/o blood transfusion requiring anemia/ and no significant family history.
Lab Work
Her Blood Pressure in clinic – AOBP(Automated office BP readings average of 3 ) was 146/92.
ABPM confirmed that she was hypertensive.
Serum Na=137,K=6,Cl=108.Creatinine=0.6, Spot Urine Protein to creatinine ratio = 0.1
ABG: Bicarb=17.9, Ph=7.32, Pco2=28, AG=11.
Spot Uk:Ucr<6, SPOT Uca:Ucr=0.7
Serum ALdosterone(PAC)=416.19 pg/ml=41.6 ng/dl
PRA=0.4ng/ml.hr
PAC/PRA=104(>30)
Diagnosis: Primary Hyperaldosteronism with Gordon’s syndrome
Discussion:
Hypertension with High PAC>10ng/dl and PAC/PRA>30, we expect a diagnosis of Primary hyperaldosteronism, in which we expect Hypokalemia, but this patient has Hyperkalemia, with Normal AG metabolic acidosis with mild Hypercalciuria, without hyperchloremia, without renal dysfunction or proteinuria.
Hyperkalemia occurs either because of shift of K from within the cells or due to renal inability to excrete. A urinary Potassium to Creatinine ratio of less than 15 indicates the hyperkalemia is due to inability of kidneys to excrete the potassium. Now common renal causes of hyperkalemia are renal
failure, Drugs like ACE-inhibitors,ARB’s,MRA’s,NSAID’s,Type 4 RTA(Hyporeninemic hypoaldosteronism), Decreased distal delivery of sodium- dehydration,NSAIDS,Heart failure or Liver failure,Gordon’s syndrome.
Hyperkalemia, here is of renal etiology, as Uk:Ucr<15, Now in Primary hyperaldosteronism we expect the overactive ENaC channels in Principal cells in CCD to reabsorb excess Sodium in exchange for Potassium, thus increased urinary potassium and hypokalemia, but if there is an activating
mutation of WNK1 or WNK4 causing over active DT reabsorbing NaCl in excess, causing less Na to reach the CCD to be exchanged for potassium, then despite of hyperaldosteronism there would be hyperkalemia due to retention of potassium. Here treatment would be to block the NaCl channel in DCT by Thiazide like diuretics so that there is increased distal delivery of Na, but the challange here is if we do that then the overactive aldosterone may cause overt hypokalemia and hypertension due to excess Aldosterone may become overt.
Treatment:
Started on Tab.Chlorthalidone 6.25mg once daily.
Tab.Sodium Bicarbonate 1000 mg once daily.
Following up.
Case 4
Interesting Case Of Glomerulonephritis:
A 60 year old diabetic for 15 years,was referred from another district, with a history of rapidly progressed renal failure requiring dialysis for almost a month for evaluaton and management.Patient had complete anuria and was dialysis dependent.
He had no systemic features of secondary GN(Vasculitis/SLE),Serology was suggestive of Low C3,normal C4, Negative ANA,ANCA,ANTI-GBM.Renal Biopsy was suggestive of Diffuse proliferative GN with IF showing only C3 deposits in the capillary walls. There was possibility of Post Infectious
GN and C3 GN.
The therapy for C3 GN would be Plasma exchange where as for PIGN it would be treating any infection if it is still active/occult.
Since the patient had no signs of infection and had sterile blood cultures, we decided to do plasma exchange while we are waiting for Electron Microscopy report to guide us about the diagnosis.
Patient received 5 sessions of PLEX and then started to slowly show improvement in his urine output, the Electron Microscopy report came as PIGN.
The patient had partial recovery of renal function after 2 months of being on dialysis, the baseline creatinine now is at 2.6.
It is a known fact that PIGN in elderly especially if at presentation if dialysis dependent then ,has very poor prognosis and unlikely to recover. What we did different in this case was PLEX. And as we know PIGN is result of an unregulated complement activation post infection leading to GN,
may be factors(Factor H,I,MCP etc) deficiency which causes the dysregulated activation of compliment activity after the infectious trigger, may be corrected by PLEX and help in recovery from PIGN,like it does in aHUS.
This is a rare case of diabetic elderly individual who is dialysis dependent for above 1 month recovering and becoming dialysis independent.