In the NEWS: Fake Nephrology Conferences and Journals: Have you have been getting these emails?

Recently, few of us have noticed we get emails inviting us to submit to " Journal .... nephrology.. and .." The best one I got one was " New England Journal of Nephrology". In addition, there are apparently these emails inviting you to be presenting at conferences that sound so real but for few of us who have been in academia- know that they are a money making scam.  What is gained from these conferences? 
Series of these conferences are run by OMICS. They are apparently for many different fields in medicine.  When I clicked on the Nephrology section for the journals, I got this

https://www.omicsonline.org/nephrology-journals.php ( mostly Non nephrology journals)
When clicked on conferences, you get these
http://www.conferenceseries.com/nephrology-meetings 

Now take a look at the locations: Las Vegas, Orlando, Dubai!!
It seems that they are happening for many years. Has anyone gone to these? Based on the NYT article that was recently published, The Federal Trade Commission formally has charged OMICS with deceiving academics and researchers on such publications and fees.

The author in the NYT says nicely at the end and I quote "So it’s not surprising that some academics have chosen to give one another permission to accumulate publication credits on their C.V.’s and spend some of the departmental travel budget on short holidays. Nor is it surprising that some canny operators have now realized that when standards are loose to begin with, there are healthy profits to be made in the gray areas of academe."

Perhaps as a community in Nephrology we need to create a page that lists which of these journals and conferences are FAKE and prevent our colleagues on spending money on these ventures.

Lupus Nephritis classification: Does it help us?

I recently went to a talk by Stephen Korbet on Lupus Nephritis and it got me wondering on if the current way of classification of lupus nephritis works or not?

MPGN- old way of classification was EM based but the recent updated IF based classification is very clinical and aids the clinician in treating the disease better as a root cause is identified.

In lupus, the story starts back in 1970s and eventually leading to the WHO classification and then the updated ISN classification. A recent review  published in JASN in 2015 summarizes the history and concerns regarding the classifications. The suggestions to improve are more detailed and pathology related and I am not sure if they will help clinically.

What might help a nephrologist help treat the lupus nephritis patient?

1. Is the lesion Proliferative?- segmental or diffuse- most of us will treat. Only context of not treating will be the IFTA present on the biopsy- so does it matter if its segmental or diffuse? as treatment is either MMF or cyclophosphamide anyway.

2. Is the lesion crescentic? - yes this matters to us-- as most crescentic GN( RPGN) and specifically lupus have been excluded in most trials- so treatment might be leaning towards cytotoxic agents and not standard therapy.

3. Is it a podocytopathy ( would like to include membranous GN in this section)- More and more we are seeing MCD, FSGS with this entity and treatment might be slightly different as some of them respond faster with a steroid based regimen.

4. Is there a second entity with it?- ANCA disease or TMA?- as treatment might then entail pheresis and or a different prognosis.


I think the talk by Korbet hinted towards this but not sure which direction the field will go but it's time that we have a less confusing classification but more meaningful one that helps the nephrologists treat the disease better.

What do others think?

Topic Discussion: Novel anticoagulants in CKD and ESRD

New Oral Anticoagulants(NOACs)	Renal clearance of parent drug	Dosage in ESRD	GFR 15-29ml/min	GFR 30-40ml/min	GFR >-50ml/min	Dialyzable (yes/no)	Reversal agent
Dabigatran( Direct thrombin inhibitor)	80%	Avoid	75mg BID	150mg BID	150mg BID	Yes with 10% rebound rate	Idarucizumab Dialysis
Rivaroxaban(Factor Xa inhibitor)	36%	15mg QD	15mg QD	15mg QD	20mg QD	No	4-factor prothrombin complex concentrate Andexanet Alfa
Apixaban( Factor Xa inhibitor)	27%	5mg BID	2.5mg BID	5mg BID	5mg BID	No	4-factor prothrombin complex concentrate Andexanet Alfa
Edoxaban (Factor Xa inhibitor)	50%	30mg QD	30mg QD	30mg QD	60mg QD	No	4-factor prothrombin complex concentrate Andexanet Alfa

Patients with atrial fibrillations are being treated with NOACs as they are simple to use, no monitoring and excellent safety profile. They are higher in costs and experience still limited. NOAC use in patients with advanced CKD and on dialysis is substantial and increasing, despite AHA, ACC, and HRS and European Heart Rhythm Association guidelines that endorse warfarin as the anticoagulant of choice when CrCl is <30 ml/min. There are few randomized trial data on NOACs among patients with advanced CKD or on dialysis. Most NOACS are dependent on the kidney for elimination. Since most patients with advanced CKD were excluded in clinical trials, this topic is important. 

The above table summarizes what the current data exists on this topic for use of NOACs in CKD patients with Atrial Fibrillation for prevention of stroke.  Bleeding risk is important in patients with CKD and ESRD due to uremic dysfunction of platelets and use of heparin in HD.  Unfortunately, no patients with CKD Stage V or ESRD were not allowed in any of the NOAC trials. Apixaban was the most commonly used NOAC in a recent analysis in advanced CKD patients. Apixaban and Rivaroxaban have renal eliminations around 30% hence most safe in late stage CKD with lower dosing. Dabigatran and Edoxaban ar 80% and 50% renal elimination respectively and should technically avoided in late CKD patients.  Dabigatran is the only NOAC removed by dialysis based on studies thus far.

This review in JACC summarizes the latest uptodate information on use of these agents in CKD and ESRD patients. – A must read!

TOPIC DISCUSSION: Is THSD7A the paraneoplastic marker for Membranous GN associated with cancer?

Two recent papers from Germany have now associated the thrombospondin type 1 domain containing 7A(THSD7A) as a target antigen identified in membranous GN  in association with cancer.   In a large study, the authors screened > 1200 patients for western blot analysis for THSD7A. The incidence was 2.6%. They were mostly women.  In this cohort, the percentage of patients with THSD7A-associated MN and malignant disease significantly exceeded that of patients with PLA₂R-associated MN and malignant disease. In all cohorts, they identified 40 patients with THSD7A-associated MN, eight of whom developed a malignancy within a median time of 3 months from diagnosis of MN. In one patient with THSD7A-associated MN and metastases of an endometrial carcinoma, immunohistochemistry showed THSD7A expression on the metastatic cells and within follicular dendritic cells of the metastasis–infiltrated lymph node. 

In a separate report in NEJM, the same group described a case of gall bladder cancer and membranous GN. The patient had circulating THSD7A antibodies and THSD7A antigen positive membranous GN.  The primary gall bladder tumor and lymph nodes also stained for THSD7A on the immunohistochemical analysis.  Following chemotherapy, the THSD7A antibodies in plasma were no longer detectable and proteinuria improved as well. In that study, when additional 1009 patients with membranous were reviewed, 25 had positive THSD7A antibodies. Of the 25, 7 had malignant tumors.

Patients with THSD7A-associated MN differ in their clinical characteristics from patients with PLA₂R1-associated MN, and more intensive screening for the presence of malignancies may be warranted in those with THSD7A-associated MN.

Topic Discussion: Serology based treatment of Membranous GN

Gone are the days of a kidney biopsy for Membranous GN… Can that happen?   Given the advent of PLAR2 antibody titers availability clinically, can we embark on a serological based approach to diagnosing and treatment of PLAR2 associated Membranous GN.  Here is a proposal from Glassock, Fervenza, Sethi  in JASN( Not evidence based at this point but pathophysiology and common sense based)

I think figures 4,5,6 summarize the entire paper nicely and are good flow charts for clinical use.

1.       Start with measurement of PLAR2 levels and screening for secondary causes.

2.       If PLAR2 is positive and no secondary cause, you have diagnosed PLAR2 associated membranous GN( perhaps no biopsy necessary—my editorial comment)

3.       If PLAR2 is negative, a kidney biopsy is mandatory ( if no contraindications and there should be PLAR2 antigen staining done on it)

4.       If PLAR2 antigen is positive on the biopsy—it’s likely a PLAR2 associated membranous GN and perhaps in immunological remission as PLAR2 antibodies were negative.  If the PLAR2 antigen in kidney is negative,   measurement of THDS7A antibody in serum and it’s antigen staining in the kidney should be performed. If that is positive, you have diagnosed THDS7A associated membranous GN and that has a strong association with cancer and hence  aggressive screening for cancer needs to be done.  IF it is PLAR2 antigen and THDS7A antigen negative but IgG subclass 3 positive, secondary causes need to be considered as this is secondary membranous GN.

5.       Once diagnosed with PLAR2 + membranous GN,  and the titer is in the high range( highest range in the respective lab), and any level of proteinuria,  the titer should be repeated twice a month and if it continues to rise, start cytotoxic agents.  If moderate PLAR2 or low and has nephrotic  or non nephrotic syndrome, again follow the titers and if rising, start treatment.  If titers are down trending or proteinuria is improving, no treatment necessary. There is going to be immunological remission before the proteinuria and clinical remission

6.       If PLAR2 AB response is rapid and >90% reduction in <6 months, consider stopping treatment

7.       If PLAR2 AB is 50% in 6 months or no response, consider changing treatment options

8.       If the response is slow (50-90%) at 6 months, continue treatment for longer time frame.

                

Topic Discussion: AKI following LVAD

Left ventricular assist devices (LVADs) are used increasingly as a bridge to transplantation or as destination therapy in end-stage heart failure patients who do not respond to optimal medical therapy. Many of these patients have end-organ dysfunction, including advanced kidney dysfunction, before and after LVAD implantation. Kidney dysfunction is a marker of adverse outcomes, such as increased morbidity and mortality.The incidence of AKI after LVAD implantation varies considerably: between 4 and 38 %. 

Risk factors:
INTERMACS score 1 or 2 ( http://content.onlinejacc.org/article.aspx?articleid=1143100)
Kidney <10 cm in size
Older age
ACE-I or ARB therapy immediately prior to surgery
High central venous pressure
Low LV end-diastolic dimensions
Long CPB time
Higher intraop bleeding
Need for re operation
Sepsis
Liver dysfunction
Need for blood transfusions
RV failure
CKD

Factors such as acute blood loss, volume shifts, arrhythmias, and the effect of multiple vasoactive medications influence renal hemodynamics. The sudden change in renal blood flow characteristics due to continuous flow-LVAD support can lead to AKI. Patients with preoperative RV failure and patients with INTERMACS scores of 1 or 2 are at higher risk of AKI.  The RV function is of vital importance after LVAD placement since postoperative RV failure and idioventricular arrhythmias have been associated with AKI . An RV dysfunction can result in a reduced LV preload, low LVAD speeds, reduced forward flow, increased arrhythmias, and liver as well as kidney congestion.

It appears that the cause is hemodynamic vs ATN. No study has really defined the mechanism. Given the LVAD devices have pro thrombotic risk , renal vascular thrombosis and or anticoagulation related AKI should be in the differential. As always, AIN from any medication is to be considered. Hemolysis related injury could be leading to pigment nephropathy as well.

https://www.ncbi.nlm.nih.gov/pubmed/25759700
https://www.ncbi.nlm.nih.gov/pubmed/25796403

Nephrology Crosswords: Hypertension

Next installment of Nephrology Crosswords appears in Kidney International in the Nov 2016 issue.
http://www.kidney-international.org/article/S0085-2538(16)30260-5/fulltext  on HTN

In the NEWS: Lung Ultrasound and volume assessment in ESRD

Your new device- the lung ultrasound has made its way in Europe. A recent trail in CJASN discusses the value of using lung ultrasound in assessing volume status of a patient.  Lung water can be used in a way in clinical practice as it is being used in critical care and cardiology to assess volume in ESRD patients.  Few prior studies that have looked at the role of ESRD and lung ultrasound in clinical practice and training of fellows/faculty  are here:

http://imaging.onlinejacc.org/article.aspx?articleid=1109604&issueno=6

http://ndt.oxfordjournals.org/content/28/11/2851.abstract?

ijkey=eebd33fc20a5ebdf81673c8b84bc28486ace19ee&keytype2=tf_ipsecsha

https://www.ncbi.nlm.nih.gov/pubmed/26880463

This new study in CJASN looked at >1000 patients pre and post HD via lung ultrasound simultaneous to standardized lung exams ( crackles ) and peripheral edema.  What the investigators found was that the lung congestion by crackles, edema or a combination was inferior to ultrasound B lines in various analysis.  Using the knowledge of B lines might guide us in better managing volume status in our ESRD patients. 

In the editorial with it in CJASN, Dr. Rich Sherman writes “I believe that lung US will prove to be of value in improving the care of patients on dialysis . From a practical standpoint, I hope that this technique can provide us with at least one simple benefit. If a routine lung US on the previous Friday before dialysis might make these events less likely, then sign me up!”

I concur with Dr Sherman! I think Nephrologists should get familiar with the science and technology and embrace this change to help their patients. Dialysis units ( large and small) should consider carrying US machines to help guide volume exam and make clinical decisions. It will decrease hospitalizations, less radiation exposure( X rays) and hopefully less ER visits.

http://www.nephronpower.com/2016/02/in-news-training-in-lung-ultrasound-for.html

http://www.nephronpower.com/2016/01/perspective-how-ultrasound-machine-has.html

Image courtesy: coreem.net

Concept Map: Electrolyte Disorders and anti cancer agents

Most electrolytes disorders are "hypo" that are drug induced from anti cancer agents. Mechanism is mentioned where there is evidence.

The two references are:
https://www.ncbi.nlm.nih.gov/pubmed/26939882
http://www.kireports.org/article/S2468-0249(16)30134-6/pdf

Topic Discussion: Complement and the Kidney

The complement system can be attacked to help treat kidney disease. Complement activation contributes to the pathogenesis of acute and chronic kidney disease injury.  The aHUS and C3GN story has led us to believe that there might be hope for other potential targets in the complement system for patients with kidney disease.

A recent mini review in KI summarizes the role of the complement system in kidney disease and where future drugs hold promise. The complement activation is initiated via 3 pathways- classical, alternative and lectin.  Full activation leads to the generation of several biologically active fragments, namely C3a, C5a, C3b and C5b-9.  Drugs are currently being developed to block the classical pathway, the alternative pathway and the activation at the level of c3,c5 and c5a.

C1 inhibitors, TNT009( anti C1s) affect the classical pathway
Purified factor H, anti Factor D agents, CR2-factor H, affect the alternative pathway
Compstatin and soluble CR1 inhibits at level of C3
Eculizumab and other anti C5 inhibit at level of C5
and CCX168 inhibits at level of C5a

Check out two excellent reviews, one in KI and other in KIR
http://www.kidney-international.org/article/S0085-2538(16)30185-5/fulltext
http://www.kireports.org/article/S2468-0249(16)30031-6/fulltext

Targeted therapies and the Kidney

Novel targeted anti-cancer therapies have resulted in improvement in patient survival compared to standard chemotherapy. Renal toxicities of targeted agents are increasingly being recognized.

The incidence, severity, and pattern of renal toxicities may vary according to the respective target of the drug. A recent uptodate review by us discusses the adverse renal effects associated with a selection of currently approved targeted cancer therapies, directed to EGFR, HER2, BRAF, MEK, ALK, PD1/PDL1, CTLA-4, and novel agents targeted to VEGF/R and TKIs.

Based on another study and look at the FDA database, electrolyte disorders, renal impairment and hypertension are the most commonly reported events with this agent. Of the novel targeted agents, ipilumumab and cetuximab have the most nephrotoxic events reported. 

Novel agents have also been tried in myeloma treatment. Renal effects of these agents are being reported as case reports and parts of clinical trials. A recent review in CJASN summaries the novel toxicities associated with new anti myeloma agents. 

The early diagnosis and prompt recognition of these renal adverse events are essential for the general nephrologist taking care of these patients.

Topic Discussion: Collapsing FSGS and TMA

Endothelial damage as a missing link… perhaps. Recent study published in KI tries to link TMA as a cause of collapsing variant of FSGS or CG.  They looked at 53 patients with renal limited TMA in a native kidney with emphasis on looking for FSGS.  33 of the 53 had FSGS( mostly 19 being CG, 9 with NOS type, 3 with cellular and rest perihalar and tip variant).  

Some interesting findings:

1.      Prognosis of TMA with FSGS was worse than TMA alone

2.      Most of the patients with TMA were from HTN followed by complement disorders, drugs and other causes. The more diffuse the TMA in the kidney in the 53 patients, the more likely they would have systemic TMA, higher crt and higher BP

3.      At the time of the renal biopsy, there was no significant difference between TMA without FSGS, TMA-CG, and TMA with other FSGS variants with respect to age, sex, and ethnicity. The degree of renal impairment also did not differ among the 3 groups. Proteinuria was significantly higher(2.5gm) in cases with FSGS (CG and other FSGS variants) than in cases without FSGS(1.42gm).  Nevertheless, there was no difference of proteinuria between CG and the “other FSGS” category (2.39 vs 2.72gm)

4.      The frequency of nephrotic syndrome was low in each group (5.9%, 11.8%, and 7.7% in “no FSGS,” CG, and “other FSGS” groups, respectively. This is interesting as FSGS classically presents with significant proteinuria.

5.      TMA associated CG and “classical” CG (i.e., CG related to ethnicity, viruses, or drugs, or a combination of these) differ on many points although they are indistinguishable by light microscopy.  Classic CG usually is seen in blacks, there they saw it in whites more.  The nephrotic syndrome is more severe in classic CG compared to TMA associated CG. Third, the authors found that dysregulation of the immunohistochemical phenotype of podocytes was less marked in our TMA-CG cases than in “classical” CG: although we observed podocyte dedifferentiation in one-half of the tested cases, proliferation of podocytes was not detected. This result is in accordance with the fact that the degree of podocyte dysregulation is less prominent in the reactive forms of CG.

6.      TMA-CG is associated with attenuated podocyte changes relative to “classical” CG and may be insufficient to trigger a full-blown clinical, immunohistochemical, and ultrastructural phenotype.

7.      Perhaps the TMA came first and led to HTN and ischemia and that leads to CG( hence the less severe proteinuria). Or is one protecting the other to keep the VEGF balance as too little VEGF leads to TMA and too much to CG.

8.      Clearly, this is an important association and finally something that can be seen in practice. Classically this is seen in HTN as it can lead to both forms of endothelial injury.

9.      Similar concepts have been noticed in post transplant CG in a prior post

http://www.nephronpower.com/2010/03/post-transplant-collapsing-fsgs-is-it.html

CONSULT ROUNDS: Glomerular disease with Sickle cell disease

From the largest case series of 18 biopsies
The four most common histology in the glomeruli were

FSGS ( 39%)-- any variant--likely due to hypoxia
MPGN(28%)- not sure if this was immuglobulin only or complement only- but likely null IF making omre likely a chronic TMA
TMA( 17%)
Sickle cell glomerulopathy( 17%)

Here is a nice recent review by Karl Nath( editor in chief of JASN)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4701210/ 

CME on Onconephrology at MD Anderson

Onconephrology Symposium at MD Anderson, Texax

When: Friday, October 14, 2016, from 8:30 am to 5:00 pm

Where: Onstead Auditorium, 6767 Bertner Ave, Houston, TX 77030

(Discounted conference rates at nearby Marriott Hotel)

Who: Healthcare professionals interested in cancer and the kidney

Topics: Nephrotoxicity of chemotherapy and targeted therapy, AKI in cancer, CKD in stem cell transplant, erythropoiesis agents, hyponatremia, hypercalcemia, ethics, dialysis and CRRT, myeloma and more!!

Speakers: Mark Perazella, Sangeeta Hingorani, Kenar Jhaveri, Ala Abudayyeh, Katy Rezvani, Steven Fishbane, Mitchell Rosner, Biff Palmer, Jennifer Scherer, Kevin Finkel, Amit Lahoti

Register at  http://tinyurl.com/MDA-Onco-Nephrology-2016

Targeted therapies and tumor lysis syndrome

Novel targeted therapies are being approved in clinical trials for many hematologic malignancies. Tumor lysis syndrome (TLS) is being noticed as a novel side effect of many of these agents. A recent review in AJH summarizes the various drugs that have led to TLS as a potential side effect of targeted therapies.

TLS was most common in drug trials dealing with patients with acute leukemias, high grade non Hodgkin’s lymphomas, mantle cell lymphomas, CLL and myeloma. Some of the risk might be tumor related rather than the drug but below are the drugs that could be potential TLS promoting.

Incidence of TLS based on clinical trials for novel targeted therapies

Alvocidib (cyclin dependent kinase inhibitor) – 42% in poor risk AML patients, 13% in CLL patients

Venetoclax( ABT-199)( small molecule B cell lymphoma/leukemia 2 inhibitor)- 2.7-8.9% in CLL

Dinaciclib( cyclin dependent kinase inhibitor)- 15% in patients with AML or ALL and another 15% in CLL

Ibrutinib( Bruton kinase inhibitor)- 6.7% in CLL patients

Dasatinib( BCR-ABL tyrosine kinase inhibitors)- 4.2% in patients with ALL

Lenalidomide( immunomodulatory agent)- 3-4% in CLL patients

Obinutuzumab( anti CD20 agent)- 3-4.8% in CLL patients

Oprozomib( proteasome inhibitor)- 2.4% in various hematologic malignancies

Brentuximab vedotin( anti cd30 antibody)- 1.7% in anaplastic large cell lymphoma patients

Carfilzomib( proteasome inhibitor)- 1% in myeloma patients

Not much found in the two listed below

Idelasib( phosphatidylinositol 3-kinase inhibitor)- No TLS in CLL patients

Ofatumumab( anti CD20 agent)-No TLS in CLL patients

Topic Discussion: Euglycemic Diabetic Ketoacidosis

The first time the term Euglycemic DKA(eDKA) was mentioned was in 1973- in British Medical Journal in patients who were diabetic but didn't have the full blown hyperglyecmic part.  Compared to classic DKA, eDKA presents with mild to moderate hyperglycemia typically <300mg/dl blood glucose levels.  

Why is this more important now?

In 2013, many SGLT2 inhibitors got approved for DM management( the glucoretics).  The FDA performed a FAERS search of adverse effects with these agents and 73 cases were identified of ketoacidosis linked to SGLT-2 inhibitors.  All patients required hospitalization, and 60% had DMII. Blood glucose levels ranged from 90mg/dl - 1300mg/dl( median 211).  Timing of onset was around 43 days or starting or dose change of the agent.  Majority of the cases also had dehydration, infection or change in insulin doses.   No mortality has been reported with this effect.  All patients respond quickly with intravenous hydration and insulin once recognized. The FDA did acknowledge that some of the cases occurred in DMI, where it's an off label use. More detail here. 



Is it a class effect? 
Yes. The initial FDA reporting was done with canagliflozin(invokana). A more recent study found an incidence rate of 0.07% with this agent.  In a large study with dapagliflozin( Farxiga), 0.1% of patients got eDKA.  Empagliflozin(Jardiance) also has been found to cause eDKA. 

What are the risk factors for development of eDKA with SGLT2 inhibitors?

Dehydration
Alcohol use
decrease in insulin use
Infection
Low carbohydrate diet
Reduction in caloric intake
Advance age

Mechanism of action

Ketosis results from restriction of carbohydrate usage with increased reliance on fat oxidation for energy production. The pathogenesis of hyperglyemic DKA is well established. Since SGLT2 are glucoretics as described before, they can lead to volume depletion- like a diuretic and perhaps leading to a "starvation" like ketoacidosis with normal glucose levels. SGLT2 induced glycosuria can happen over 24 hours and this artificial low plasma glucose do not stimulate insulin. In eDKA, insulin deficiency and insulin resistance are milder; therefore, glucose overproduction and under-utilization are quantitatively lesser than in DKA. More importantly, renal glucose clearance (i.e., the ratio of glycosuria to prevailing glycemia) is twice as large with eDKA than with DKA. Ketoacidosis follows with the same sequence of events in eDKA as in DKA. Insufficient insulin levels will then decrease glucose utilization and promote lipolysis and ketogenesis. In addition, these drugs can increase glucagon levels leading to increase ketone production.

In summary, eDKA is pathophysiologically similar to DKA except for the circumstance—SGLT2-induced glycosuria—that “artificially” lowers plasma glucose levels and predisposes to increased ketogenesis.

Prevention and treatment
Blood and urine monitoring of ketones is essential especially when patients get ill or are experiencing one of the risk factors.  Adequate hydration and carbohydrate intake will help and holding the offending agent is indicated.  No data exists on a safe time to restart the agent. 

Here is a nice review on this topic
http://onlinelibrary.wiley.com/doi/10.1111/jdi.12401/pdf

Detective Nephron: the next case

Check out the next venture of Detective Nephron in the August issue of Kidney News 2016

http://www.kidneynews.org/kidney-news/features/detective-nephron-world-renowned-for-expert-analytical-skills-trains-budding-physician-detectives-on

TOPIC DISCUSSION: New anti retrovirals and the kidney

As HIV becomes a chronic illness, novel agents to combat this virus have been out in the last decade. We are familiar with the renal toxicities of tenofivir for many years. Tenofivir is the cisplatin of the ID world.  But what about the new novel agents?
Here is a table that summarizes the new agents and their known or unknown renal toxicities

Drug name( trade)	Mechanism of Action	Renal effect	Excretion	Reference
Rilpivirine(Edurant)	Non nucleoside reverse transcriptase inhibitor	Decreases the secretion of creatinine in the proximal tubule via OCT2 , appear after 1-2 weeks after treatment and can then plateau	Renal	https://www.ncbi.nlm.nih.gov/pubmed/23211772 https://www.ncbi.nlm.nih.gov/pubmed/21763936
Dolutegravir(Tivicay)	Integrase inhibitor	Decreases the secretion of creatinine in the proximal tubule via OCT2, appear 1-2 weeks after treatment and then plateau	Liver	https://www.ncbi.nlm.nih.gov/pubmed/22905856
Cobicistat(Tybost)	Inhibitor liver enzymes so other HIV drugs effect gets enhanced	Decreases in secretion of creatinine  in the apical side of proximal tubule as it inhibits MATE 1 transporter, can be as early as day 7 of start.	Liver	https://www.ncbi.nlm.nih.gov/pubmed/22732469

Tenofivir dispoxil fumarate( TDF) is the classic nephrotoxic agent.  It actively taken up by the proximal tubular cell via OAT1 and 3 and released in urinary space by secretion of MDRP-2 and 4. There is a novel tenofivir formulation called tenofivir alafenamide fumrate( TAF) which is used in lower dosage combinations and lower level of parent drug is noted. In addition, TAF does not bind to these organic transporters and hence less renal tubular trafficking. Once out in clinical use, we might see less tenofivir related renal toxicities. 

A lot of combination agents are being used to combat the virus. The list below from FDA approved AIDS website compiles them with their trade names. The most nephrotoxic ones are the ones that contain TDF as expected or one of the above mentioned agents that block creatinine secretion.

abacavir and lamivudine (abacavir sulfate / lamivudine, ABC / 3TC)	Epzicom	No renal concerns
abacavir, dolutegravir, and lamivudine (abacavir sulfate / dolutegravir sodium / lamivudine, ABC / DTG / 3TC)	Triumeq	Slight increase in creatinine
abacavir, lamivudine, and zidovudine (abacavir sulfate / lamivudine / zidovudine, ABC / 3TC / ZDV)	Trizivir	No renal concerns
atazanavir and cobicistat (atazanavir sulfate / cobicistat, ATV / COBI)	Evotaz	Slight increase in creatinine
darunavir and cobicistat (darunavir ethanolate / cobicistat, DRV / COBI)	Prezcobix	Slight increase in creatinine
efavirenz, emtricitabine, and tenofovir disoproxil fumarate (efavirenz / emtricitabine / tenofovir, efavirenz / emtricitabine / tenofovir DF, EFV / FTC / TDF)	Atripla	Contains tenofivir- renal toxicity can be present
elvitegravir, cobicistat, emtricitabine, and tenofovir alafenamide fumarate (elvitegravir / cobicistat / emtricitabine / tenofovir alafenamide, EVG / COBI / FTC / TAF)	Genvoya	Contains tenofivir
elvitegravir, cobicistat, emtricitabine, and tenofovir disoproxil fumarate (QUAD, EVG / COBI / FTC / TDF)	Stribild	Contains tenofivir
emtricitabine, rilpivirine, and tenofovir alafenamide (emtricitabine / rilpivirine / tenofovir AF, emtricitabine / rilpivirine / tenofovir alafenamide fumarate, emtricitabine / rilpivirine hydrochloride / tenofovir AF, emtricitabine / rilpivirine hydrochloride / tenofovir alafenamide, emtricitabine / rilpivirine hydrochloride / tenofovir alafenamide fumarate, FTC / RPV / TAF)	Odefsey	Tenofvir alafenamide does not bind to the proximal tubule transporters and is potentially less nephrotoxic
emtricitabine, rilpivirine, and tenofovir disoproxil fumarate (emtricitabine / rilpivirine hydrochloride / tenofovir disoproxil fumarate, emtricitabine / rilpivirine / tenofovir, FTC / RPV / TDF)	Complera	Contains tenofivir- hence renal failure can occur and rilpivirine can increase crt as well
emtricitabine and tenofovir alafenamide (emtricitabine / tenofovir AF, emtricitabine / tenofovir alafenamide fumarate, FTC / TAF)	Descovy	Novel tenovifir- hence less likely
emtricitabine and tenofovir disoproxil fumarate (emtricitabine / tenofovir, FTC / TDF)	Truvada	Can cause AKI given tenofivir presence
lamivudine and zidovudine (3TC / ZDV)	Combivir	No renal issues
lopinavir and ritonavir (ritonavir-boosted lopinavir, LPV/r, LPV / RTV)	Kaletra	No renal issues